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<article article-type="research-article" dtd-version="1.3" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xml:lang="ru"><front><journal-meta><journal-id journal-id-type="publisher-id">pulmo</journal-id><journal-title-group><journal-title xml:lang="ru">Пульмонология</journal-title><trans-title-group xml:lang="en"><trans-title>PULMONOLOGIYA</trans-title></trans-title-group></journal-title-group><issn pub-type="ppub">0869-0189</issn><issn pub-type="epub">2541-9617</issn><publisher><publisher-name>Scientific and Practical Journal “PULMONOLOGIYA” LLC</publisher-name></publisher></journal-meta><article-meta><article-id pub-id-type="doi">10.18093/0869-0189-2022-3108</article-id><article-id custom-type="elpub" pub-id-type="custom">pulmo-3108</article-id><article-categories><subj-group subj-group-type="heading"><subject>Research Article</subject></subj-group><subj-group subj-group-type="section-heading" xml:lang="ru"><subject>ОБЗОРЫ</subject></subj-group><subj-group subj-group-type="section-heading" xml:lang="en"><subject>REVIEW</subject></subj-group></article-categories><title-group><article-title>Клеточный метаболизм и дисфункция митохондрий при хронической обструктивной болезни легких</article-title><trans-title-group xml:lang="en"><trans-title>Cellular metabolism and mitochondrial dysfunction in chronic obstructive pulmonary disease</trans-title></trans-title-group></title-group><contrib-group><contrib contrib-type="author" corresp="yes"><contrib-id contrib-id-type="orcid">https://orcid.org/0000-0002-0117-0349</contrib-id><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Невзорова</surname><given-names>В. А.</given-names></name><name name-style="western" xml:lang="en"><surname>Nevzorova</surname><given-names>V. A.</given-names></name></name-alternatives><bio xml:lang="ru"><p>Невзорова Вера Афанасьевна – доктор медицинских наук, профессор, директор Института терапии и инструментальной диагностики Тихоокеанский ГМУ, главный внештатный специалист по терапии Дальневосточного федерального округа.</p><p>690002, Владивосток, пр-т Острякова, 2; тел.: (423) 240-23-63</p></bio><bio xml:lang="en"><p>Vera A. Nevzorova - Doctor of Medicine, Professor, Director, Institute of Therapy and Instrumental Diagnostics, Pacific SMU, Chief External Therapeutist, Far Eastern Federal District.</p><p>pr. Ostryakova 2, Vladivostok, 690002; tel.: (423) 240-23-63</p></bio><email xlink:type="simple">nevzorova@inbox.ru</email><xref ref-type="aff" rid="aff-1"/></contrib><contrib contrib-type="author" corresp="yes"><contrib-id contrib-id-type="orcid">https://orcid.org/0000-0002-9836-6339</contrib-id><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Бродская</surname><given-names>Т. А.</given-names></name><name name-style="western" xml:lang="en"><surname>Brodskaya</surname><given-names>T. A.</given-names></name></name-alternatives><bio xml:lang="ru"><p>Бродская Татьяна Александровна – доктор медицинских наук, профессор Института терапии и инструментальной диагностики.</p><p>690002, Владивосток, пр-т Острякова, 2; тел.: (423) 45-26-38</p></bio><bio xml:lang="en"><p>Tat’yana A. Brodskaya - Doctor of Medicine, Professor, Institute of Therapy and Instrumental Diagnostics.</p><p>pr. Ostryakova 2, Vladivostok, 690002; tel.: (423) 45-26-38</p></bio><email xlink:type="simple">brodskaya@mail.ru</email><xref ref-type="aff" rid="aff-1"/></contrib><contrib contrib-type="author" corresp="yes"><contrib-id contrib-id-type="orcid">https://orcid.org/0000-0002-8701-7213</contrib-id><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Плехова</surname><given-names>Н. Г.</given-names></name><name name-style="western" xml:lang="en"><surname>Plekhova</surname><given-names>N. G.</given-names></name></name-alternatives><bio xml:lang="ru"><p>Плехова Наталья Геннадьевна – доктор биологических наук, заведующая Центральной научно-исследовательской лабораторией.</p><p>690002, Владивосток, пр-т Острякова, 2; тел.: (423) 240-23-63</p></bio><bio xml:lang="en"><p>Natal’ya G. Plekhova - Doctor of Biology, Head of the Central Research Laboratory.</p><p>pr. Ostryakova 2, Vladivostok, 690002; tel.: (423) 240-23-63</p></bio><email xlink:type="simple">pl_nat@hotmail.com</email><xref ref-type="aff" rid="aff-1"/></contrib><contrib contrib-type="author" corresp="yes"><contrib-id contrib-id-type="orcid">https://orcid.org/0000-0002-3946-2064</contrib-id><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Присеко</surname><given-names>Л. Г.</given-names></name><name name-style="western" xml:lang="en"><surname>Priseko</surname><given-names>L. G.</given-names></name></name-alternatives><bio xml:lang="ru"><p>Присеко Людмила Григорьевна – аспирант, ассистент Института терапии и инструментальной диагностики.</p><p>690002, Владивосток, пр-т Острякова, 2; тел.: (423) 45-26-38</p></bio><bio xml:lang="en"><p>Lyudmila G. Priseko - Postgraduate student, Assistant, Institute of Therapy and Instrumental Diagnostics.</p><p>pr. Ostryakova 2, Vladivostok, 690002; tel.: (423) 45-26-38</p></bio><email xlink:type="simple">ludmilka.95.95@yandex.ru</email><xref ref-type="aff" rid="aff-1"/></contrib><contrib contrib-type="author" corresp="yes"><contrib-id contrib-id-type="orcid">https://orcid.org/0000-0002-7231-3001</contrib-id><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Евстифеева</surname><given-names>А. А.</given-names></name><name name-style="western" xml:lang="en"><surname>Evstifeeva</surname><given-names>A. A.</given-names></name></name-alternatives><bio xml:lang="ru"><p>Евстифеева Анастасия Алексеевна – врач-пульмонолог пульмонологического отделения.</p><p>690078, Приморский край, Владивосток, ул. Садовая, 22; тел.: (423) 245-28-36</p></bio><bio xml:lang="en"><p>Anastasiya A. Evstifeeva - Pulmonologist, Pulmonology Department.</p><p>ul. Sadovaya 22, Vladivostok, 690078; tel.: (423) 245-28-36</p></bio><email xlink:type="simple">evstifeevaanastasiya@mail.ru</email><xref ref-type="aff" rid="aff-2"/></contrib><contrib contrib-type="author" corresp="yes"><contrib-id contrib-id-type="orcid">https://orcid.org/0000-0001-8602-0691</contrib-id><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Багирова</surname><given-names>А. Э.</given-names></name><name name-style="western" xml:lang="en"><surname>Bagirova</surname><given-names>A. E.</given-names></name></name-alternatives><bio xml:lang="ru"><p>Багирова Айнура Эльчин кызы – врач-кардиолог отделения неотложной кардиологии.</p><p>690078, Приморский край, Владивосток, ул. Садовая, 22; тел.: (423) 245-28-36</p></bio><bio xml:lang="en"><p>Aynura E. Bagirova - Cardiologist, Department of Emergency Cardiology.</p><p>ul. Sadovaya 22, Vladivostok, 690078; tel.: (423) 245-28-36</p></bio><email xlink:type="simple">bagira.nura@mail.ru</email><xref ref-type="aff" rid="aff-2"/></contrib></contrib-group><aff-alternatives id="aff-1"><aff xml:lang="ru"><institution>Федеральное государственное бюджетное образовательное учреждение высшего образования Тихоокеанский государственный медицинский университет, Министерство здравоохранения Российской Федерации</institution><country>Россия</country></aff><aff xml:lang="en"><institution>Federal State Budgetary Educational Institution of Higher Education Pacific State Medical University, Ministry of Health of the Russian Federation</institution><country>Russian Federation</country></aff></aff-alternatives><aff-alternatives id="aff-2"><aff xml:lang="ru"><institution>Краевое государственное бюджетное учреждение здравоохранения Владивостокская клиническая больница № 1</institution><country>Россия</country></aff><aff xml:lang="en"><institution>Regional State Budgetary Healthcare Institution Vladivostok Clinical Hospital No.1</institution><country>Russian Federation</country></aff></aff-alternatives><pub-date pub-type="collection"><year>2023</year></pub-date><pub-date pub-type="epub"><day>11</day><month>02</month><year>2023</year></pub-date><volume>33</volume><issue>1</issue><fpage>84</fpage><lpage>91</lpage><permissions><copyright-statement>Copyright &amp;#x00A9; Невзорова В.А., Бродская Т.А., Плехова Н.Г., Присеко Л.Г., Евстифеева А.А., Багирова А.Э., 2023</copyright-statement><copyright-year>2023</copyright-year><copyright-holder xml:lang="ru">Невзорова В.А., Бродская Т.А., Плехова Н.Г., Присеко Л.Г., Евстифеева А.А., Багирова А.Э.</copyright-holder><copyright-holder xml:lang="en">Nevzorova V.A., Brodskaya T.A., Plekhova N.G., Priseko L.G., Evstifeeva A.A., Bagirova A.E.</copyright-holder><license xml:lang="ru" license-type="creative-commons-attribution" xlink:href="https://creativecommons.org/licenses/by/4.0/" xlink:type="simple"><license-p>Данная работа распространяется под лицензией Creative Commons Attribution 4.0.</license-p></license><license xml:lang="en" license-type="creative-commons-attribution" xlink:href="https://creativecommons.org/licenses/by/4.0/" xlink:type="simple"><license-p>This work is licensed under a Creative Commons Attribution 4.0 License.</license-p></license></permissions><self-uri xlink:href="https://journal.pulmonology.ru/pulm/article/view/3108">https://journal.pulmonology.ru/pulm/article/view/3108</self-uri><abstract><p>Хроническая обструктивная болезнь легких (ХОБЛ) в силу многообразия и системности проявлений рассматривается в качестве типичной модели ускоренного старения. К ведущему фактору тканевого ремоделирования при ХОБЛ относятся изменение клеточного метаболизма или его перепрограммирование в ответ на воздействие таких внешних факторов, как продукты сгорания табака, биотопливо, вирусы и др. Среди многообразия механизмов тканевого и клеточного перепрограммирования при ХОБЛ доминирующую позицию занимают вопросы митоходриальной биологии. Являясь парасимбиотическими органеллами, митохондрии имеют сложную систему взаимодействия с клетками целостного организма и участвуют в процессах как биогенеза, или образования новых органелл, так и митофагии, или удаления клеткой-хозяином дефектных митохондрий. При ХОБЛ происходит дизрегуляция обоих этих механизмов.</p><p>Целью обзора явилось объединение накопленного научно-исследовательского опыта в области изучения клеточного метаболизма и роли митохондрий для углубленного фенотипирования ХОБЛ в зависимости от вариантов метаболического перепрограммирования и создания новых терапевтических возможностей для их коррекции.</p><p>Заключение. Митохондрии являются ключевыми регуляторами метаболизма, окислительно-восстановительного гомеостаза, выживания и пролиферации клеток. Указанные процессы, контролируемые разнообразными путями внутри- и межклеточного сигналинга, демонстрируют дисбаланс при ХОБЛ на уровне различных тканевых дифферонов: альвеолоцитов, эпителиальных клеток легочной ткани, гладких миоцитов дыхательных путей, альвеолярных макрофагов, поперечнополосатой мускулатуры, мезенхимальных стромальных клеток, прогениторных клеток и пр. Результаты, полученные при изучении метаболома и митохондриальной функции, формируют идеи для поиска новых терапевтических возможностей в терапии ХОБЛ.</p></abstract><trans-abstract xml:lang="en"><p>Chronic obstructive pulmonary disease (COPD) is considered a typical model of accelerated aging due to the variability and systemic nature of its manifestations. The leading factor in tissue remodeling in COPD is a change or reprogramming of the cellular metabolism in response to external factors such as tobacco combustion products, biofuels, viruses, etc. Mitochondrial biology dominates the spectrum of mechanisms of tissue and cellular reprogramming in COPD. Being parasymbiotic organelles, mitochondria have a complex system of interaction with other cells of the human body and participate in both biogenesis, or formation of new organelles, and mitophagy, or elimination of defective mitochondria by the host cell. Both of these mechanisms are dysregulated in COPD.</p><p>The aim of this work is to combine the accumulated research experience in the field of cellular metabolism and the role of mitochondria for in-depth COPD phenotyping depending on the metabolic reprogramming variants and for development of new therapeutic possibilities to correct the reprogramming.</p><p>Conclusion. Mitochondria are key regulators of metabolism, redox homeostasis, cell survival and proliferation. These processes are controlled by various intra- and intercellular signaling pathways and reflect the COPD-associated imbalance at the level of various tissue lineages: alveolocytes, epithelial cells of the lung tissue, smooth myocytes of the respiratory tract, alveolar macrophages, striated muscle cells, mesenchymal stromal cells, progenitor cells, etc. The studies of metabolome and mitochondrial function pointed out where to look for new therapeutic options for COPD.</p></trans-abstract><kwd-group xml:lang="ru"><kwd>хроническая обструктивная болезнь легких</kwd><kwd>митохондрии</kwd><kwd>митохондриальная дисфункция</kwd><kwd>клеточный метаболизм</kwd><kwd>метаболом перепрограммирования</kwd></kwd-group><kwd-group xml:lang="en"><kwd>chronic obstructive pulmonary disease</kwd><kwd>mitochondria</kwd><kwd>mitochondrial dysfunction</kwd><kwd>cell metabolism</kwd><kwd>reprogramming metabolome</kwd></kwd-group><funding-group><funding-statement xml:lang="ru">Спонсорская поддержка отсутствовала</funding-statement><funding-statement xml:lang="en">The study was not sponsored</funding-statement></funding-group></article-meta></front><back><ref-list><title>References</title><ref id="cit1"><label>1</label><citation-alternatives><mixed-citation xml:lang="ru">Бродская Т.А., Невзорова В.А., Васильева М.С., Лавренюк В.В. Нейроопосредованные и эндотелийзависимые механизмы формирования хронической обструктивной болезни легких. Терапевтический архив. 2020; 92 (3): 116–124. DOI: 10.26442/00403660.2020.03.000347.</mixed-citation><mixed-citation xml:lang="en">Brodskaya T.A., Nevzorova V.A., Vasileva M.S., Lavrenyuk V.V. [Endothelium-related and neuro-mediated mechanisms of emphysema development in chronic obstructive pulmonary disease]. Terapevticheskiy arkhiv. 2020; 92 (3): 116–124. DOI: 10.26442/00403660.2020.03.000347 (in Russian).</mixed-citation></citation-alternatives></ref><ref id="cit2"><label>2</label><citation-alternatives><mixed-citation xml:lang="ru">Nevzorova V., Brodskaya T., Gilifanov E. Smoking and COPD: Endothelium-related and neuro-mediated emphysema mechanisms. In: Herrera Garcia J.C., ed. Respiratory disease update. London: IntechOpen; 2020. DOI: 10.5772/intechopen.85927.</mixed-citation><mixed-citation xml:lang="en">Nevzorova V., Brodskaya T., Gilifanov E. Smoking and COPD: Endothelium-related and neuro-mediated emphysema mechanisms. In: Herrera Garcia J.C., ed. Respiratory disease update. London: IntechOpen; 2020. DOI: 10.5772/intechopen.85927.</mixed-citation></citation-alternatives></ref><ref id="cit3"><label>3</label><citation-alternatives><mixed-citation xml:lang="ru">MacNee W., Rabinovich R.A., Choudhury G. Ageing and the border between health and disease. Eur. Respir. J. 2014; 44 (5): 1332–1352. DOI: 10.1183/09031936.00134014.</mixed-citation><mixed-citation xml:lang="en">MacNee W., Rabinovich R.A., Choudhury G. Ageing and the border between health and disease. Eur. Respir. J. 2014; 44 (5): 1332–1352. DOI: 10.1183/09031936.00134014.</mixed-citation></citation-alternatives></ref><ref id="cit4"><label>4</label><citation-alternatives><mixed-citation xml:lang="ru">Hiemstra P.S., van der Does A.M. Reprogramming of cellular metabolism: driver for airway remodelling in COPD? Eur. Respir. J. 2017; 50 (5): 1702197. DOI: 10.1183/13993003.02197-2017.</mixed-citation><mixed-citation xml:lang="en">Hiemstra P.S., van der Does A.M. Reprogramming of cellular metabolism: driver for airway remodelling in COPD? Eur. Respir. J. 2017; 50 (5): 1702197. DOI: 10.1183/13993003.02197-2017.</mixed-citation></citation-alternatives></ref><ref id="cit5"><label>5</label><citation-alternatives><mixed-citation xml:lang="ru">Naz S., Kolmert J., Yang M. et al. Metabolomics analysis identifies sex-associated metabotypes of oxidative stress and the autotaxin-lysoPA axis in COPD. Eur. Respir. J. 2017; 49 (6): 1602322. DOI: 10.1183/13993003.02322-2016.</mixed-citation><mixed-citation xml:lang="en">Naz S., Kolmert J., Yang M. et al. Metabolomics analysis identifies sex-associated metabotypes of oxidative stress and the autotaxin-lysoPA axis in COPD. Eur. Respir. J. 2017; 49 (6): 1602322. DOI: 10.1183/13993003.02322-2016.</mixed-citation></citation-alternatives></ref><ref id="cit6"><label>6</label><citation-alternatives><mixed-citation xml:lang="ru">López-Otín C., Blasco M.A., Partridge L. et al. The hallmarks of ageing. Cell. 2013; 153 (6): 1194–1217. DOI: 10.1016/j.cell.2013.05.039.</mixed-citation><mixed-citation xml:lang="en">López-Otín C., Blasco M.A., Partridge L. et al. The hallmarks of ageing. Cell. 2013; 153 (6): 1194–1217. DOI: 10.1016/j.cell.2013.05.039.</mixed-citation></citation-alternatives></ref><ref id="cit7"><label>7</label><citation-alternatives><mixed-citation xml:lang="ru">Cloonan S.M., Kim K., Esteves P. et al. Mitochondrial dysfunction in lung ageing and disease. Eur. Respir. Rev. 2020; 29 (157): 200165. DOI: 10.1183/16000617.0165-2020.</mixed-citation><mixed-citation xml:lang="en">Cloonan S.M., Kim K., Esteves P. et al. Mitochondrial dysfunction in lung ageing and disease. Eur. Respir. Rev. 2020; 29 (157): 200165. DOI: 10.1183/16000617.0165-2020.</mixed-citation></citation-alternatives></ref><ref id="cit8"><label>8</label><citation-alternatives><mixed-citation xml:lang="ru">Мережковский К.С. Теория двух плазм как основа симбиогенезиса, нового учения о происхождении организмов. Казань: Типография Императорского университета; 1909. Доступно на: https://elib.rgo.ru/handle/123456789/231019</mixed-citation><mixed-citation xml:lang="en">Merezhkovskiy K.S. [The Theory of Two Plasmas as the Basis of Symbiogenesis, a New Study or the Origins of Organisms]. Kazan: Tipografiya Imperatorskogo universiteta; 1909. Available at: https://elib.rgo.ru/handle/123456789/231019 (in Russian).</mixed-citation></citation-alternatives></ref><ref id="cit9"><label>9</label><citation-alternatives><mixed-citation xml:lang="ru">Sagan L. On the origin of mitosing cells. J. Theor. Biol. 1967; 14 (3): 255–274. DOI: 10.1016/0022-5193(67)90079-3.</mixed-citation><mixed-citation xml:lang="en">Sagan L. On the origin of mitosing cells. J. Theor. Biol. 1967; 14 (3): 255–274. DOI: 10.1016/0022-5193(67)90079-3.</mixed-citation></citation-alternatives></ref><ref id="cit10"><label>10</label><citation-alternatives><mixed-citation xml:lang="ru">Mishra P., Carelli V., Manfredi G., Chan D.C. Proteolytic cleavage of Opa1 stimulates mitochondrial inner membrane fusion and couples fusion to oxidative phosphorylation. Cell Metab. 2014; 19 (4): 630–641. DOI: 10.1016/j.cmet.2014.03.011.</mixed-citation><mixed-citation xml:lang="en">Mishra P., Carelli V., Manfredi G., Chan D.C. Proteolytic cleavage of Opa1 stimulates mitochondrial inner membrane fusion and couples fusion to oxidative phosphorylation. Cell Metab. 2014; 19 (4): 630–641. DOI: 10.1016/j.cmet.2014.03.011.</mixed-citation></citation-alternatives></ref><ref id="cit11"><label>11</label><citation-alternatives><mixed-citation xml:lang="ru">Toyama E.Q., Herzig S., Courchet J. et al. Metabolism. AMP-activated protein kinase mediates mitochondrial fission in response to energy stress. Science. 2016; 351 (6270): 275–281. DOI: 10.1126/science.aab4138.</mixed-citation><mixed-citation xml:lang="en">Toyama E.Q., Herzig S., Courchet J. et al. Metabolism. AMP-activated protein kinase mediates mitochondrial fission in response to energy stress. Science. 2016; 351 (6270): 275–281. DOI: 10.1126/science.aab4138.</mixed-citation></citation-alternatives></ref><ref id="cit12"><label>12</label><citation-alternatives><mixed-citation xml:lang="ru">Mishra P., Chan D.C. Mitochondrial dynamics and inheritance during cell division, development and disease. Nat. Rev. Mol. Cell Biol. 2014; 15 (10): 634–646. DOI: 10.1038/nrm3877.</mixed-citation><mixed-citation xml:lang="en">Mishra P., Chan D.C. Mitochondrial dynamics and inheritance during cell division, development and disease. Nat. Rev. Mol. Cell Biol. 2014; 15 (10): 634–646. DOI: 10.1038/nrm3877.</mixed-citation></citation-alternatives></ref><ref id="cit13"><label>13</label><citation-alternatives><mixed-citation xml:lang="ru">Mizumura K., Cloonan S.M., Nakahira K. et al. Mitophagy-dependent necroptosis contributes to the pathogenesis of COPD. J. Clin. Invest. 2014; 124 (9): 3987–4003. DOI: 10.1172/JCI74985.</mixed-citation><mixed-citation xml:lang="en">Mizumura K., Cloonan S.M., Nakahira K. et al. Mitophagy-dependent necroptosis contributes to the pathogenesis of COPD. J. Clin. Invest. 2014; 124 (9): 3987–4003. DOI: 10.1172/JCI74985.</mixed-citation></citation-alternatives></ref><ref id="cit14"><label>14</label><citation-alternatives><mixed-citation xml:lang="ru">Kovarova M., Hesker P.R., Jania L. et al. NLRP1-dependent pyroptosis leads to acute lung injury and morbidity in mice. J. Immunol. 2012; 189 (4): 2006–2016. DOI: 10.4049/jimmunol.1201065.</mixed-citation><mixed-citation xml:lang="en">Kovarova M., Hesker P.R., Jania L. et al. NLRP1-dependent pyroptosis leads to acute lung injury and morbidity in mice. J. Immunol. 2012; 189 (4): 2006–2016. DOI: 10.4049/jimmunol.1201065.</mixed-citation></citation-alternatives></ref><ref id="cit15"><label>15</label><citation-alternatives><mixed-citation xml:lang="ru">Cloonan S.M., Choi A.M. Mitochondria in lung disease. J. Clin. Invest. 2016; 126 (3): 809–820. DOI: 10.1172/JCI81113.</mixed-citation><mixed-citation xml:lang="en">Cloonan S.M., Choi A.M. Mitochondria in lung disease. J. Clin. Invest. 2016; 126 (3): 809–820. DOI: 10.1172/JCI81113.</mixed-citation></citation-alternatives></ref><ref id="cit16"><label>16</label><citation-alternatives><mixed-citation xml:lang="ru">Hoffmann R.F., Zarrintan S., Brandenburg S.M. et al. Prolonged cigarette smoke exposure alters mitochondrial structure and function in airway epithelial cells. Respir. Res. 2013; 14 (1): 97. DOI: 10.1186/1465-9921-14-97.</mixed-citation><mixed-citation xml:lang="en">Hoffmann R.F., Zarrintan S., Brandenburg S.M. et al. Prolonged cigarette smoke exposure alters mitochondrial structure and function in airway epithelial cells. Respir. Res. 2013; 14 (1): 97. DOI: 10.1186/1465-9921-14-97.</mixed-citation></citation-alternatives></ref><ref id="cit17"><label>17</label><citation-alternatives><mixed-citation xml:lang="ru">Wiegman C.H., Michaeloudes C., Haji G. et al. Oxidative stress-induced mitochondrial dysfunction drives inflammation and airway smooth muscle remodeling in patients with chronic obstructive pulmonary disease. J. Allergy Clin. Immunol. 2015; 136 (3): 769–780. DOI: 10.1016/j.jaci.2015.01.046.</mixed-citation><mixed-citation xml:lang="en">Wiegman C.H., Michaeloudes C., Haji G. et al. Oxidative stress-induced mitochondrial dysfunction drives inflammation and airway smooth muscle remodeling in patients with chronic obstructive pulmonary disease. J. Allergy Clin. Immunol. 2015; 136 (3): 769–780. DOI: 10.1016/j.jaci.2015.01.046.</mixed-citation></citation-alternatives></ref><ref id="cit18"><label>18</label><citation-alternatives><mixed-citation xml:lang="ru">Tennant D.A., Durán R.V., Gottlieb E. Targeting metabolic transformation for cancer therapy. Nat. Rev. Cancer. 2010; 10 (4): 267–277. DOI: 10.1038/nrc2817.</mixed-citation><mixed-citation xml:lang="en">Tennant D.A., Durán R.V., Gottlieb E. Targeting metabolic transformation for cancer therapy. Nat. Rev. Cancer. 2010; 10 (4): 267–277. DOI: 10.1038/nrc2817.</mixed-citation></citation-alternatives></ref><ref id="cit19"><label>19</label><citation-alternatives><mixed-citation xml:lang="ru">Michaeloudes C., Kuo C.H., Haji G. et al. Metabolic re-patterning in COPD airway smooth muscle cells. Eur. Respir. J. 2017; 50 (5): 1700202. DOI: 10.1183/13993003.00202-2017.</mixed-citation><mixed-citation xml:lang="en">Michaeloudes C., Kuo C.H., Haji G. et al. Metabolic re-patterning in COPD airway smooth muscle cells. Eur. Respir. J. 2017; 50 (5): 1700202. DOI: 10.1183/13993003.00202-2017.</mixed-citation></citation-alternatives></ref><ref id="cit20"><label>20</label><citation-alternatives><mixed-citation xml:lang="ru">Aravamudan B., Kiel A., Freeman M. et al. Cigarette smoke-induced mitochondrial fragmentation and dysfunction in human airway smooth muscle. Am. J. Physiol. Lung Cell. Mol. Physiol. 2014; 306 (9): L840–854. DOI: 10.1152/ajplung.00155.2013.</mixed-citation><mixed-citation xml:lang="en">Aravamudan B., Kiel A., Freeman M. et al. Cigarette smoke-induced mitochondrial fragmentation and dysfunction in human airway smooth muscle. Am. J. Physiol. Lung Cell. Mol. Physiol. 2014; 306 (9): L840–854. DOI: 10.1152/ajplung.00155.2013.</mixed-citation></citation-alternatives></ref><ref id="cit21"><label>21</label><citation-alternatives><mixed-citation xml:lang="ru">Aravamudan B., Thompson M., Sieck G.C. et al. Functional effects of cigarette smoke-induced changes in airway smooth muscle mitochondrial morphology. J. Cell. Physiol. 2017; 232 (5): 1053–1068. DOI: 10.1002/jcp.25508.</mixed-citation><mixed-citation xml:lang="en">Aravamudan B., Thompson M., Sieck G.C. et al. Functional effects of cigarette smoke-induced changes in airway smooth muscle mitochondrial morphology. J. Cell. Physiol. 2017; 232 (5): 1053–1068. DOI: 10.1002/jcp.25508.</mixed-citation></citation-alternatives></ref><ref id="cit22"><label>22</label><citation-alternatives><mixed-citation xml:lang="ru">Kirkham P.A., Barnes P.J. Oxidative stress in COPD. Chest. 2013; 144 (1): 266–273. DOI: 10.1378/chest.12-2664.</mixed-citation><mixed-citation xml:lang="en">Kirkham P.A., Barnes P.J. Oxidative stress in COPD. Chest. 2013; 144 (1): 266–273. DOI: 10.1378/chest.12-2664.</mixed-citation></citation-alternatives></ref><ref id="cit23"><label>23</label><citation-alternatives><mixed-citation xml:lang="ru">Bernstein L.H. The role of mitochondrial imbalance in pulmonary diseases. EC Pulmonol. Respir. Med. 2019; 8 (4): 336–344. Available at: https://ecronicon.com/ecprm/pdf/ECPRM-08-00362.pdf</mixed-citation><mixed-citation xml:lang="en">Bernstein L.H. The role of mitochondrial imbalance in pulmonary diseases. EC Pulmonol. Respir. Med. 2019; 8 (4): 336–344. Available at: https://ecronicon.com/ecprm/pdf/ECPRM-08-00362.pdf</mixed-citation></citation-alternatives></ref><ref id="cit24"><label>24</label><citation-alternatives><mixed-citation xml:lang="ru">Wu G., Zhu Q., Zeng J. et al. Extracellular mitochondrial DNA promote NLRP3 inflammasome activation and induce acute lung injury through TLR9 and NF-κB. J. Thorac. Dis. 2019; 11 (11): 4816–4828. DOI: 10.21037/jtd.2019.10.26.</mixed-citation><mixed-citation xml:lang="en">Wu G., Zhu Q., Zeng J. et al. Extracellular mitochondrial DNA promote NLRP3 inflammasome activation and induce acute lung injury through TLR9 and NF-κB. J. Thorac. Dis. 2019; 11 (11): 4816–4828. DOI: 10.21037/jtd.2019.10.26.</mixed-citation></citation-alternatives></ref><ref id="cit25"><label>25</label><citation-alternatives><mixed-citation xml:lang="ru">West A.P., Khoury-Hanold W., Staron M. et al. Mitochondrial DNA stress primes the antiviral innate immune response. Nature. 2015; 520 (7548): 553–557. DOI: 10.1038/nature14156.</mixed-citation><mixed-citation xml:lang="en">West A.P., Khoury-Hanold W., Staron M. et al. Mitochondrial DNA stress primes the antiviral innate immune response. Nature. 2015; 520 (7548): 553–557. DOI: 10.1038/nature14156.</mixed-citation></citation-alternatives></ref><ref id="cit26"><label>26</label><citation-alternatives><mixed-citation xml:lang="ru">Robb E.L., Hall A.R., Prime T.A. et al. Control of mitochondrial superoxide production by reverse electron transport at complex I. J. Biol. Chem. 2018; 293 (25): 9869–9879. DOI: 10.1074/jbc.RA118.003647.</mixed-citation><mixed-citation xml:lang="en">Robb E.L., Hall A.R., Prime T.A. et al. Control of mitochondrial superoxide production by reverse electron transport at complex I. J. Biol. Chem. 2018; 293 (25): 9869–9879. DOI: 10.1074/jbc.RA118.003647.</mixed-citation></citation-alternatives></ref><ref id="cit27"><label>27</label><citation-alternatives><mixed-citation xml:lang="ru">Brand M.D. Mitochondrial generation of superoxide and hydrogen peroxide as the source of mitochondrial redox signaling. Free Radic Biol. Med. 2016; 100: 14–31. DOI: 10.1016/j.freeradbiomed.2016.04.001.</mixed-citation><mixed-citation xml:lang="en">Brand M.D. Mitochondrial generation of superoxide and hydrogen peroxide as the source of mitochondrial redox signaling. Free Radic Biol. Med. 2016; 100: 14–31. DOI: 10.1016/j.freeradbiomed.2016.04.001.</mixed-citation></citation-alternatives></ref><ref id="cit28"><label>28</label><citation-alternatives><mixed-citation xml:lang="ru">Ryter S.W., Rosas I.O., Owen C.A. et al. Mitochondrial dysfunction as a pathogenic mediator of chronic obstructivepulmonary disease and idiopathic pulmonary fibrosis. Ann. Am. Thorac. Soc. 2018; 15 (Suppl. 4): S266–272. DOI: 10.1513/AnnalsATS.201808-585MG.</mixed-citation><mixed-citation xml:lang="en">Ryter S.W., Rosas I.O., Owen C.A. et al. Mitochondrial dysfunction as a pathogenic mediator of chronic obstructivepulmonary disease and idiopathic pulmonary fibrosis. Ann. Am. Thorac. Soc. 2018; 15 (Suppl. 4): S266–272. DOI: 10.1513/AnnalsATS.201808-585MG.</mixed-citation></citation-alternatives></ref><ref id="cit29"><label>29</label><citation-alternatives><mixed-citation xml:lang="ru">Xu F., Wen Z., Shi X., Fan J. Inflammasome in the pathogenesis of pulmonary diseases. Exp. Suppl. 2018; 108: 111–151. DOI: 10.1007/978-3-319-89390-7_6.</mixed-citation><mixed-citation xml:lang="en">Xu F., Wen Z., Shi X., Fan J. Inflammasome in the pathogenesis of pulmonary diseases. Exp. Suppl. 2018; 108: 111–151. DOI: 10.1007/978-3-319-89390-7_6.</mixed-citation></citation-alternatives></ref><ref id="cit30"><label>30</label><citation-alternatives><mixed-citation xml:lang="ru">Kang M.J., Shadel G.S. A mitochondrial perspective of chronic obstructive pulmonary disease pathogenesis. Tuberc. Respir. Dis. 2016; 79 (4): 207–213. DOI: 10.4046/trd.2016.79.4.207.</mixed-citation><mixed-citation xml:lang="en">Kang M.J., Shadel G.S. A mitochondrial perspective of chronic obstructive pulmonary disease pathogenesis. Tuberc. Respir. Dis. 2016; 79 (4): 207–213. DOI: 10.4046/trd.2016.79.4.207.</mixed-citation></citation-alternatives></ref><ref id="cit31"><label>31</label><citation-alternatives><mixed-citation xml:lang="ru">Kang M.J., Yoon C.M., Kim B.H. et al. Suppression of NLRX1 in chronic obstructive pulmonary disease. J. Clin. Invest. 2015; 125 (6): 2458–2462. DOI: 10.1172/JCI71747.</mixed-citation><mixed-citation xml:lang="en">Kang M.J., Yoon C.M., Kim B.H. et al. Suppression of NLRX1 in chronic obstructive pulmonary disease. J. Clin. Invest. 2015; 125 (6): 2458–2462. DOI: 10.1172/JCI71747.</mixed-citation></citation-alternatives></ref><ref id="cit32"><label>32</label><citation-alternatives><mixed-citation xml:lang="ru">Yoon C.M., Nam M., Oh Y.M. et al. Mitochondrial regulation of inflammasome activation in chronic obstructive pulmonary disease. J. Innate Immun. 2016; 8 (2): 121–128. DOI: 10.1159/000441299.</mixed-citation><mixed-citation xml:lang="en">Yoon C.M., Nam M., Oh Y.M. et al. Mitochondrial regulation of inflammasome activation in chronic obstructive pulmonary disease. J. Innate Immun. 2016; 8 (2): 121–128. DOI: 10.1159/000441299.</mixed-citation></citation-alternatives></ref><ref id="cit33"><label>33</label><citation-alternatives><mixed-citation xml:lang="ru">Cloonan S.M., Glass K., Laucho-Contreras M.E. et al. Mitochondrial iron chelation ameliorates cigarette smoke-induced bronchitis and emphysema in mice. Nat. Med. 2016; 22 (2): 163–174. DOI: 10.1038/nm.4021.</mixed-citation><mixed-citation xml:lang="en">Cloonan S.M., Glass K., Laucho-Contreras M.E. et al. Mitochondrial iron chelation ameliorates cigarette smoke-induced bronchitis and emphysema in mice. Nat. Med. 2016; 22 (2): 163–174. DOI: 10.1038/nm.4021.</mixed-citation></citation-alternatives></ref><ref id="cit34"><label>34</label><citation-alternatives><mixed-citation xml:lang="ru">Barnes P.J., Baker J., Donnelly L.E. Cellular senescence as a mechanism and target in chronic lung diseases. Am. J. Respir. Crit. Care Med. 2019; 200 (5): 556–564. DOI: 10.1164/rccm.201810-1975TR.</mixed-citation><mixed-citation xml:lang="en">Barnes P.J., Baker J., Donnelly L.E. Cellular senescence as a mechanism and target in chronic lung diseases. Am. J. Respir. Crit. Care Med. 2019; 200 (5): 556–564. DOI: 10.1164/rccm.201810-1975TR.</mixed-citation></citation-alternatives></ref><ref id="cit35"><label>35</label><citation-alternatives><mixed-citation xml:lang="ru">Zhu Y., Liu X., Ding X. et al. Telomere and its role in the aging pathways: telomere shortening, cell senescence and mitochondria dysfunction. Biogerontology. 2019; 20 (1): 1–16. DOI: 10.1007/s10522018-9769-1.</mixed-citation><mixed-citation xml:lang="en">Zhu Y., Liu X., Ding X. et al. Telomere and its role in the aging pathways: telomere shortening, cell senescence and mitochondria dysfunction. Biogerontology. 2019; 20 (1): 1–16. DOI: 10.1007/s10522018-9769-1.</mixed-citation></citation-alternatives></ref><ref id="cit36"><label>36</label><citation-alternatives><mixed-citation xml:lang="ru">van der Rijt S., Molenaars M., McIntyre R.L. et al. Integrating the hallmarks of aging throughout the tree of life: a focus on mitochondrial dysfunction. Front. Cell Dev. Biol. 2020; 8: 594416. DOI: 10.3389/fcell.2020.594416.</mixed-citation><mixed-citation xml:lang="en">van der Rijt S., Molenaars M., McIntyre R.L. et al. Integrating the hallmarks of aging throughout the tree of life: a focus on mitochondrial dysfunction. Front. Cell Dev. Biol. 2020; 8: 594416. DOI: 10.3389/fcell.2020.594416.</mixed-citation></citation-alternatives></ref><ref id="cit37"><label>37</label><citation-alternatives><mixed-citation xml:lang="ru">Subramaniam K., Kumar H., Tawhai M.H. Evidence for age-dependent air-space enlargement contributing to loss of lung tissue elastic recoil pressure and increased shear modulus in older age. J. Appl. Physiol. (1985). 2017; 123 (1): 79–87. DOI: 10.1152/japplphysiol.00208.2016.</mixed-citation><mixed-citation xml:lang="en">Subramaniam K., Kumar H., Tawhai M.H. Evidence for age-dependent air-space enlargement contributing to loss of lung tissue elastic recoil pressure and increased shear modulus in older age. J. Appl. Physiol. (1985). 2017; 123 (1): 79–87. DOI: 10.1152/japplphysiol.00208.2016.</mixed-citation></citation-alternatives></ref><ref id="cit38"><label>38</label><citation-alternatives><mixed-citation xml:lang="ru">Sahin E., DePinho R.A. Axis of ageing: telomeres, p53 and mitochondria. Nat. Rev. Mol. Cell Biol. 2012; 13 (6): 397–404. DOI: 10.1038/nrm3352.</mixed-citation><mixed-citation xml:lang="en">Sahin E., DePinho R.A. Axis of ageing: telomeres, p53 and mitochondria. Nat. Rev. Mol. Cell Biol. 2012; 13 (6): 397–404. DOI: 10.1038/nrm3352.</mixed-citation></citation-alternatives></ref><ref id="cit39"><label>39</label><citation-alternatives><mixed-citation xml:lang="ru">Mercado N., Colley T., Baker J.R. et al. Bicaudal D1 impairs autophagosome maturation in chronic obstructive pulmonary disease. FASEB Bioadv. 2019; 1 (11): 688–705. DOI: 10.1096/fba.2018-00055.</mixed-citation><mixed-citation xml:lang="en">Mercado N., Colley T., Baker J.R. et al. Bicaudal D1 impairs autophagosome maturation in chronic obstructive pulmonary disease. FASEB Bioadv. 2019; 1 (11): 688–705. DOI: 10.1096/fba.2018-00055.</mixed-citation></citation-alternatives></ref><ref id="cit40"><label>40</label><citation-alternatives><mixed-citation xml:lang="ru">Kelly G. A review of the sirtuin system, its clinical implications, and the potential role of dietary activators like resveratrol: part 1. Altern. Med. Rev. 2010; 15 (3): 245–263. Available at: https://altmedrev.com/blog/resource/a-review-of-the-sirtuin-system-its-clinical-implications-and-the-potential-role-of-dietary-activators-like-resveratrol-part-1/</mixed-citation><mixed-citation xml:lang="en">Kelly G. A review of the sirtuin system, its clinical implications, and the potential role of dietary activators like resveratrol: part 1. Altern. Med. Rev. 2010; 15 (3): 245–263. Available at: https://altmedrev.com/blog/resource/a-review-of-the-sirtuin-system-its-clinical-implications-and-the-potential-role-of-dietary-activators-like-resveratrol-part-1/</mixed-citation></citation-alternatives></ref><ref id="cit41"><label>41</label><citation-alternatives><mixed-citation xml:lang="ru">Takasaka N., Araya J., Hara H. et al. Autophagy induction by SIRT6 through attenuation of insulin-like growth factor signaling is involved in the regulation of human bronchial epithelial cell senescence. J. Immunol. 2014; 192 (3): 958–968. DOI: 10.4049/jimmunol.1302341.</mixed-citation><mixed-citation xml:lang="en">Takasaka N., Araya J., Hara H. et al. Autophagy induction by SIRT6 through attenuation of insulin-like growth factor signaling is involved in the regulation of human bronchial epithelial cell senescence. J. Immunol. 2014; 192 (3): 958–968. DOI: 10.4049/jimmunol.1302341.</mixed-citation></citation-alternatives></ref><ref id="cit42"><label>42</label><citation-alternatives><mixed-citation xml:lang="ru">To M., Takagi D., Akashi K. et al. Sputum plasminogen activator inhibitor-1 elevation by oxidative stress-dependent nuclear factor-kappaB activation in COPD. Chest. 2013; 144 (2): 515–521. DOI: 10.1378/chest.12-2381.</mixed-citation><mixed-citation xml:lang="en">To M., Takagi D., Akashi K. et al. Sputum plasminogen activator inhibitor-1 elevation by oxidative stress-dependent nuclear factor-kappaB activation in COPD. Chest. 2013; 144 (2): 515–521. DOI: 10.1378/chest.12-2381.</mixed-citation></citation-alternatives></ref><ref id="cit43"><label>43</label><citation-alternatives><mixed-citation xml:lang="ru">Ahmad T., Sundar I.K., Lerner C.A. et al. Impaired mitophagy leads to cigarette smoke stress-induced cellular senescence: implications for chronic obstructive pulmonary disease. FASEB J. 2015; 29 (7): 2912–2929. DOI: 10.1096/fj.14-268276.</mixed-citation><mixed-citation xml:lang="en">Ahmad T., Sundar I.K., Lerner C.A. et al. Impaired mitophagy leads to cigarette smoke stress-induced cellular senescence: implications for chronic obstructive pulmonary disease. FASEB J. 2015; 29 (7): 2912–2929. DOI: 10.1096/fj.14-268276.</mixed-citation></citation-alternatives></ref><ref id="cit44"><label>44</label><citation-alternatives><mixed-citation xml:lang="ru">Szczesny B., Marcatti M., Ahmad A. et al. Mitochondrial DNA damage and subsequent activation of Z-DNA binding protein 1 links oxidative stress to inflammation in epithelial cells. Sci. Rep. 2018; 8 (1): 914. DOI: 10.1038/s41598-018-19216-1.</mixed-citation><mixed-citation xml:lang="en">Szczesny B., Marcatti M., Ahmad A. et al. Mitochondrial DNA damage and subsequent activation of Z-DNA binding protein 1 links oxidative stress to inflammation in epithelial cells. Sci. Rep. 2018; 8 (1): 914. DOI: 10.1038/s41598-018-19216-1.</mixed-citation></citation-alternatives></ref><ref id="cit45"><label>45</label><citation-alternatives><mixed-citation xml:lang="ru">Zhang W.Z., Rice M.C., Hoffman K.L. et al. Association of urine mitochondrial DNA with clinical measures of COPD in the SPIROMICS cohort. JCI Insight. 2020; 5 (3): e133984. DOI: 10.1172/jci.insight.133984.</mixed-citation><mixed-citation xml:lang="en">Zhang W.Z., Rice M.C., Hoffman K.L. et al. Association of urine mitochondrial DNA with clinical measures of COPD in the SPIROMICS cohort. JCI Insight. 2020; 5 (3): e133984. DOI: 10.1172/jci.insight.133984.</mixed-citation></citation-alternatives></ref><ref id="cit46"><label>46</label><citation-alternatives><mixed-citation xml:lang="ru">Lazaar A.L., Greenhaff P.L. Impaired muscle mitochondrial density and/or function: a COPD-specific mitochondropathy or simply deconditioning? Eur. Respir. J. 2012; 40 (5): 1070–1071. DOI: 10.1183/09031936.00051012.</mixed-citation><mixed-citation xml:lang="en">Lazaar A.L., Greenhaff P.L. Impaired muscle mitochondrial density and/or function: a COPD-specific mitochondropathy or simply deconditioning? Eur. Respir. J. 2012; 40 (5): 1070–1071. DOI: 10.1183/09031936.00051012.</mixed-citation></citation-alternatives></ref><ref id="cit47"><label>47</label><citation-alternatives><mixed-citation xml:lang="ru">Meyer A., Zoll J., Charles A.L. et al. Skeletal muscle mitochondrial dysfunction during chronic obstructive pulmonary disease: central actor and therapeutic target. Exp. Physiol. 2013; 98 (6): 1063–1078. DOI: 10.1113/expphysiol.2012.069468.</mixed-citation><mixed-citation xml:lang="en">Meyer A., Zoll J., Charles A.L. et al. Skeletal muscle mitochondrial dysfunction during chronic obstructive pulmonary disease: central actor and therapeutic target. Exp. Physiol. 2013; 98 (6): 1063–1078. DOI: 10.1113/expphysiol.2012.069468.</mixed-citation></citation-alternatives></ref><ref id="cit48"><label>48</label><citation-alternatives><mixed-citation xml:lang="ru">Taivassalo T., Hussain S.N. Contribution of the mitochondria to locomotor muscle dysfunction in patients with COPD. Chest. 2016; 149 (5): 1302–1312. DOI: 10.1016/j.chest.2015.11.021.</mixed-citation><mixed-citation xml:lang="en">Taivassalo T., Hussain S.N. Contribution of the mitochondria to locomotor muscle dysfunction in patients with COPD. Chest. 2016; 149 (5): 1302–1312. DOI: 10.1016/j.chest.2015.11.021.</mixed-citation></citation-alternatives></ref><ref id="cit49"><label>49</label><citation-alternatives><mixed-citation xml:lang="ru">Dillon L.M., Rebelo A.P., Moraes C.T. The role of PGC-1 coactivators in aging skeletal muscle and heart. IUBMB Life. 2012; 64 (3): 231–241. DOI: 10.1002/iub.608.</mixed-citation><mixed-citation xml:lang="en">Dillon L.M., Rebelo A.P., Moraes C.T. The role of PGC-1 coactivators in aging skeletal muscle and heart. IUBMB Life. 2012; 64 (3): 231–241. DOI: 10.1002/iub.608.</mixed-citation></citation-alternatives></ref><ref id="cit50"><label>50</label><citation-alternatives><mixed-citation xml:lang="ru">Belchamber K.B.R., Singh R., Batista C.M. et al. Defective bacterial phagocytosis is associated with dysfunctional mitochondria in COPD macrophages. Eur. Respir. J. 2019; 54 (4): 1802244. DOI: 10.1183/13993003.02244-2018.</mixed-citation><mixed-citation xml:lang="en">Belchamber K.B.R., Singh R., Batista C.M. et al. Defective bacterial phagocytosis is associated with dysfunctional mitochondria in COPD macrophages. Eur. Respir. J. 2019; 54 (4): 1802244. DOI: 10.1183/13993003.02244-2018.</mixed-citation></citation-alternatives></ref><ref id="cit51"><label>51</label><citation-alternatives><mixed-citation xml:lang="ru">Ubags N.D., Baker J., Boots A. et al. ERS International Congress, Madrid, 2019: highlights from the Basic and Translational Science Assembly. ERJ Open Res. 2020; 6 (1): 00350-2019 DOI: 10.1183/23120541.00350-2019.</mixed-citation><mixed-citation xml:lang="en">Ubags N.D., Baker J., Boots A. et al. ERS International Congress, Madrid, 2019: highlights from the Basic and Translational Science Assembly. ERJ Open Res. 2020; 6 (1): 00350-2019 DOI: 10.1183/23120541.00350-2019.</mixed-citation></citation-alternatives></ref><ref id="cit52"><label>52</label><citation-alternatives><mixed-citation xml:lang="ru">Weinberg S.E., Sena L.A., Chandel N.S. Mitochondria in the regulation of innate and adaptive immunity. Immunity. 2015; 42 (3): 406–417. DOI: 10.1016/j.immuni.2015.02.002.</mixed-citation><mixed-citation xml:lang="en">Weinberg S.E., Sena L.A., Chandel N.S. Mitochondria in the regulation of innate and adaptive immunity. Immunity. 2015; 42 (3): 406–417. DOI: 10.1016/j.immuni.2015.02.002.</mixed-citation></citation-alternatives></ref><ref id="cit53"><label>53</label><citation-alternatives><mixed-citation xml:lang="ru">Sun C., Liu X., Wang B. et al. Endocytosis-mediated mitochondrial transplantation: Transferring normal human astrocytic mitochondria into glioma cells rescues aerobic respiration and enhances radiosensitivity. Theranostics. 2019; 9 (12): 3595–3607. DOI: 10.7150/thno.33100.</mixed-citation><mixed-citation xml:lang="en">Sun C., Liu X., Wang B. et al. Endocytosis-mediated mitochondrial transplantation: Transferring normal human astrocytic mitochondria into glioma cells rescues aerobic respiration and enhances radiosensitivity. Theranostics. 2019; 9 (12): 3595–3607. DOI: 10.7150/thno.33100.</mixed-citation></citation-alternatives></ref><ref id="cit54"><label>54</label><citation-alternatives><mixed-citation xml:lang="ru">Jackson M.V., Morrison T.J., Doherty D.F., McAuley D.F. Mitochondrial transfer via tunneling nanotubes is an important mechanism by which mesenchymal stem cells enhance macrophage phagocytosis in the in vitro and in vivo models of ARDS. Stem. Cells. 2016; 34 (8): 2210–2223. DOI: 10.1002/stem.2372.</mixed-citation><mixed-citation xml:lang="en">Jackson M.V., Morrison T.J., Doherty D.F., McAuley D.F. Mitochondrial transfer via tunneling nanotubes is an important mechanism by which mesenchymal stem cells enhance macrophage phagocytosis in the in vitro and in vivo models of ARDS. Stem. Cells. 2016; 34 (8): 2210–2223. DOI: 10.1002/stem.2372.</mixed-citation></citation-alternatives></ref><ref id="cit55"><label>55</label><citation-alternatives><mixed-citation xml:lang="ru">Van den Bossche J., O’Neill L.A., Menon D. Macrophage immunometabolism: where are we (going)? Trends Immunol. 2017; 38 (6): 395–406. DOI: 10.1016/j.it.2017.03.001.</mixed-citation><mixed-citation xml:lang="en">Van den Bossche J., O’Neill L.A., Menon D. Macrophage immunometabolism: where are we (going)? Trends Immunol. 2017; 38 (6): 395–406. DOI: 10.1016/j.it.2017.03.001.</mixed-citation></citation-alternatives></ref><ref id="cit56"><label>56</label><citation-alternatives><mixed-citation xml:lang="ru">O’Beirne S.L., Kikkers S.A., Oromendia C. et al. Alveolar macrophage immunometabolism and lung function impairment in smoking and chronic obstructive pulmonary disease. Am. J. Respir. Crit. Care Med. 2020; 201 (6): 735–739. DOI: 10.1164/rccm.201908-1683LE.</mixed-citation><mixed-citation xml:lang="en">O’Beirne S.L., Kikkers S.A., Oromendia C. et al. Alveolar macrophage immunometabolism and lung function impairment in smoking and chronic obstructive pulmonary disease. Am. J. Respir. Crit. Care Med. 2020; 201 (6): 735–739. DOI: 10.1164/rccm.201908-1683LE.</mixed-citation></citation-alternatives></ref><ref id="cit57"><label>57</label><citation-alternatives><mixed-citation xml:lang="ru">Xie Z.Z., Liu Y., Bian J.S. Hydrogen sulfide and cellular redox homeostasis. Oxid. Med. Cell. Longev. 2016; 2016: 6043038. DOI: 10.1155/2016/6043038.</mixed-citation><mixed-citation xml:lang="en">Xie Z.Z., Liu Y., Bian J.S. Hydrogen sulfide and cellular redox homeostasis. Oxid. Med. Cell. Longev. 2016; 2016: 6043038. DOI: 10.1155/2016/6043038.</mixed-citation></citation-alternatives></ref><ref id="cit58"><label>58</label><citation-alternatives><mixed-citation xml:lang="ru">Sun Y., Wang K., Li M.X. et al. Metabolic changes of H2S in smokers and patients of COPD which might involve in inflammation, oxidative stress and steroid sensitivity. Sci. Rep. 2015; 5: 14971. DOI: 10.1038/srep14971.</mixed-citation><mixed-citation xml:lang="en">Sun Y., Wang K., Li M.X. et al. Metabolic changes of H2S in smokers and patients of COPD which might involve in inflammation, oxidative stress and steroid sensitivity. Sci. Rep. 2015; 5: 14971. DOI: 10.1038/srep14971.</mixed-citation></citation-alternatives></ref><ref id="cit59"><label>59</label><citation-alternatives><mixed-citation xml:lang="ru">He Y., Liu S., Zhang Z. et al. Imbalance of endogenous hydrogen sulfide and homocysteine in chronic obstructive pulmonary disease combined with cardiovascular disease. Front. Pharmacol. 2017; 8: 624. DOI: 10.3389/fphar.2017.00624.</mixed-citation><mixed-citation xml:lang="en">He Y., Liu S., Zhang Z. et al. Imbalance of endogenous hydrogen sulfide and homocysteine in chronic obstructive pulmonary disease combined with cardiovascular disease. Front. Pharmacol. 2017; 8: 624. DOI: 10.3389/fphar.2017.00624.</mixed-citation></citation-alternatives></ref><ref id="cit60"><label>60</label><citation-alternatives><mixed-citation xml:lang="ru">Beckett E.L., Stevens R.L., Jarnicki A.G. et al. A new short-term mouse model of chronic obstructive pulmonary disease identifies a role for mast cell tryptase in pathogenesis. J. Allergy Clin. Immunol. 2013; 131 (3): 752–762. DOI: 10.1016/j.jaci.2012.11.053.</mixed-citation><mixed-citation xml:lang="en">Beckett E.L., Stevens R.L., Jarnicki A.G. et al. A new short-term mouse model of chronic obstructive pulmonary disease identifies a role for mast cell tryptase in pathogenesis. J. Allergy Clin. Immunol. 2013; 131 (3): 752–762. DOI: 10.1016/j.jaci.2012.11.053.</mixed-citation></citation-alternatives></ref><ref id="cit61"><label>61</label><citation-alternatives><mixed-citation xml:lang="ru">Mills E.L., Ryan D.G., Prag H.A. et al. Itaconate is an anti-inflammatory metabolite that activates Nrf2 via alkylation of KEAP1. Nature. 2018: 556 (7699): 113–117. DOI: 10.1038/nature25986.</mixed-citation><mixed-citation xml:lang="en">Mills E.L., Ryan D.G., Prag H.A. et al. Itaconate is an anti-inflammatory metabolite that activates Nrf2 via alkylation of KEAP1. Nature. 2018: 556 (7699): 113–117. DOI: 10.1038/nature25986.</mixed-citation></citation-alternatives></ref><ref id="cit62"><label>62</label><citation-alternatives><mixed-citation xml:lang="ru">Hara H., Araya J., Ito S. et al. Mitochondrial fragmentation in cigarette smoke-induced bronchial epithelial cell senescence. Am. J. Physiol. Lung Cell. Mol. Physiol. 2013; 305 (10): L737–746. DOI: 10.1152/ajplung.00146.2013.</mixed-citation><mixed-citation xml:lang="en">Hara H., Araya J., Ito S. et al. Mitochondrial fragmentation in cigarette smoke-induced bronchial epithelial cell senescence. Am. J. Physiol. Lung Cell. Mol. Physiol. 2013; 305 (10): L737–746. DOI: 10.1152/ajplung.00146.2013.</mixed-citation></citation-alternatives></ref><ref id="cit63"><label>63</label><citation-alternatives><mixed-citation xml:lang="ru">Ogger P.P., Silva J.D., Aghapour M. et al. Early career members at the ERS lung science conference 2020: metabolic alterations in lung ageing and disease. Breathe (Sheff.). 2020; 16 (3): 200063. DOI: 10.1183/20734735.0063-2020.</mixed-citation><mixed-citation xml:lang="en">Ogger P.P., Silva J.D., Aghapour M. et al. Early career members at the ERS lung science conference 2020: metabolic alterations in lung ageing and disease. Breathe (Sheff.). 2020; 16 (3): 200063. DOI: 10.1183/20734735.0063-2020.</mixed-citation></citation-alternatives></ref><ref id="cit64"><label>64</label><citation-alternatives><mixed-citation xml:lang="ru">Michaeloudes C., Bhavsar P.K., Mumby S. et al. Role of metabolic reprogramming in pulmonary innate immunity and its impact on lung diseases. J. Innate Immun. 2020; 12 (1): 31–46. DOI: 10.1159/000504344.</mixed-citation><mixed-citation xml:lang="en">Michaeloudes C., Bhavsar P.K., Mumby S. et al. Role of metabolic reprogramming in pulmonary innate immunity and its impact on lung diseases. J. Innate Immun. 2020; 12 (1): 31–46. DOI: 10.1159/000504344.</mixed-citation></citation-alternatives></ref></ref-list><fn-group><fn fn-type="conflict"><p>The authors declare that there are no conflicts of interest present.</p></fn></fn-group></back></article>
