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<article article-type="review-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">vmireaviz</journal-id><journal-title-group><journal-title xml:lang="ru">Вестник медицинского института «РЕАВИЗ». Реабилитация, Врач и Здоровье</journal-title><trans-title-group xml:lang="en"><trans-title>Bulletin of the Medical Institute "REAVIZ" (REHABILITATION, DOCTOR AND HEALTH)</trans-title></trans-title-group></journal-title-group><issn pub-type="ppub">2226-762X</issn><issn pub-type="epub">2782-1579</issn><publisher><publisher-name>РЕАВИЗ</publisher-name></publisher></journal-meta><article-meta><article-id pub-id-type="doi">10.20340/vmi-rvz.2026.2.CLIN.6</article-id><article-id custom-type="elpub" pub-id-type="custom">vmireaviz-1700</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>Клиническая медицина</subject></subj-group><subj-group subj-group-type="section-heading" xml:lang="en"><subject>Clinical medicine</subject></subj-group></article-categories><title-group><article-title>Митохондриальная сеть как ключевое звено выживаемости нейроваскулярной единицы</article-title><trans-title-group xml:lang="en"><trans-title>The mitochondrial network as a key link in the survival of the neurovascular unit</trans-title></trans-title-group></title-group><contrib-group><contrib contrib-type="author" corresp="yes"><contrib-id contrib-id-type="orcid">https://orcid.org/0000-0002-9238-8270</contrib-id><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Сороковикова</surname><given-names>Т. В.</given-names></name><name name-style="western" xml:lang="en"><surname>Sorokovikova</surname><given-names>T. V.</given-names></name></name-alternatives><bio xml:lang="ru"><p>Сороковикова Татьяна Викторовна - Канд. мед. наук, доцент, доцент кафедры неврологии, реабилитации и нейрохирургии</p><p>ул. Советская, д. 4, г. Тверь, 170100, Россия</p></bio><bio xml:lang="en"><p>Tat'yana V. Sorokovikova - Cand. Sci. (Med.), Docent, Associate Professor of the Department of Neurology, Rehabilitation, and Neurosurgery</p><p>Sovetskaya St., 4, Tver, 170100, Russia</p></bio><xref ref-type="aff" rid="aff-1"/></contrib><contrib contrib-type="author" corresp="yes"><contrib-id contrib-id-type="orcid">https://orcid.org/0000-0002-8055-1958</contrib-id><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Павлова</surname><given-names>О. Н.</given-names></name><name name-style="western" xml:lang="en"><surname>Pavlova</surname><given-names>O. N.</given-names></name></name-alternatives><bio xml:lang="ru"><p>Павлова Ольга Николаевна - Д-р биол. наук, доцент, заведующий кафедрой физиологии</p><p>ул. Чапаевская, д. 89, г. Самара, 443099, Россия</p></bio><bio xml:lang="en"><p>Ol'ga N. Pavlova - Dr. Sci. (Biol.), Docent, Head of the  Department of Physiology</p><p> Chapaevskaya St., 89, Samara, 443099, Russia </p></bio><email xlink:type="simple">casiopeya13@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/0000-0001-6338-7095</contrib-id><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Гуленко</surname><given-names>О. Н.</given-names></name><name name-style="western" xml:lang="en"><surname>Gulenko</surname><given-names>O. N.</given-names></name></name-alternatives><bio xml:lang="ru"><p>Гуленко Ольга Николаевна - Канд. биол. наук, доцент, доцент кафедры физиологии</p><p>ул. Чапаевская, д. 89, г. Самара, 443099, Россия</p></bio><bio xml:lang="en"><p>Ol'ga N. Gulenko - Cand. Sci. (Biol.), Docent, Associate Professor of the Department of Physiology</p><p>Chapaevskaya St., 89, Samara, 443099, Russia</p></bio><xref ref-type="aff" rid="aff-2"/></contrib></contrib-group><aff-alternatives id="aff-1"><aff xml:lang="ru"><institution>Тверской государственный медицинский университет</institution><country>Россия</country></aff><aff xml:lang="en"><institution>Tver State Medical University</institution><country>Russian Federation</country></aff></aff-alternatives><aff-alternatives id="aff-2"><aff xml:lang="ru"><institution>Самарский государственный медицинский университет</institution><country>Россия</country></aff><aff xml:lang="en"><institution>Samara State Medical University</institution><country>Russian Federation</country></aff></aff-alternatives><pub-date pub-type="collection"><year>2026</year></pub-date><pub-date pub-type="epub"><day>15</day><month>07</month><year>2026</year></pub-date><volume>16</volume><issue>2</issue><fpage>86</fpage><lpage>98</lpage><permissions><copyright-statement>Copyright &amp;#x00A9; Сороковикова Т.В., Павлова О.Н., Гуленко О.Н., 2026</copyright-statement><copyright-year>2026</copyright-year><copyright-holder xml:lang="ru">Сороковикова Т.В., Павлова О.Н., Гуленко О.Н.</copyright-holder><copyright-holder xml:lang="en">Sorokovikova T.V., Pavlova O.N., Gulenko O.N.</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://vestnik.reaviz.ru/jour/article/view/1700">https://vestnik.reaviz.ru/jour/article/view/1700</self-uri><abstract><p>Обзор посвящён анализу фундаментальных механизмов деградации и восстановления нейроваскулярной единицы (НВЕ) в условиях острого дефицита церебрального кровотока и последующей реперфузии. Рассматриваются физиологические основы клеточной дезорганизации, где ведущим фактором деструкции нейрональных мембран выступает липопероксидация. Особое внимание уделено роли митохондриальной сети как центрального регулятора выживаемости клеток НВЕ. В работе подробно описываются современные представления о структурно-функциональной целостности НВЕ и молекулярных механизмах её повреждения. Центральное место занимает анализ регуляторной оси PGC-1α как ключевого фактора митохондриального биогенеза и антиоксидантной защиты. Авторы систематизируют данные о процессах митохондриальной динамики (слияния), селективной аутофагии (митофагии) и роли неспецифической митохондриальной поры (mPTP) в определении судьбы клеток в постперфузионном периоде. В заключительной части обзора обсуждаются перспективные стратегии фармакологической коррекции: от купирования оксидативного стресса и нейровоспаления до индукции биогенеза органелл. Обосновывается терапевтический потенциал модуляции митохондриального пула как эффективного метода восстановления нейроваскулярной единицы после ишемического поражения.</p></abstract><trans-abstract xml:lang="en"><p>This review analyzes the fundamental mechanisms of neurovascular unit (NVU) degradation and restoration under conditions of acute cerebral blood flow deficiency and subsequent reperfusion. The physiological basis of cellular disorganization is examined, with lipid peroxidation acting as the leading factor in neuronal membrane destruction. Particular attention is paid to the role of the mitochondrial network as a central regulator of NVU cell survival. The paper describes in detail current understanding of the structural and functional integrity of the NVU and the molecular mechanisms of its damage. Central to this is the analysis of the PGC-1α regulatory axis as a key factor in mitochondrial biogenesis and antioxidant defense. The authors systematize data on mitochondrial dynamics (fusion), selective autophagy (mitophagy), and the role of the mitochondrial proliferator-activated pore (mPTP) in determining cell fate in the post-perfusion period. The final section of the review discusses promising strategies for pharmacological correction: from the reduction of oxidative stress and neuroinflammation to the induction of organelle biogenesis. The therapeutic potential of mitochondrial modulation as an effective method for restoring the neurovascular unit after ischemic injury is substantiated.</p></trans-abstract><kwd-group xml:lang="ru"><kwd>нейроваскулярная</kwd><kwd>ишемия-реперфузия головного мозга</kwd><kwd>митохондриальный биогенез</kwd><kwd>PGC-1α</kwd><kwd>оксидативный</kwd><kwd>митофагия</kwd><kwd>митохондриальная пора</kwd><kwd>нейропротекция</kwd></kwd-group><kwd-group xml:lang="en"><kwd>neurovascular unit</kwd><kwd>cerebral ischemia-reperfusion</kwd><kwd>mitochondrial biogenesis</kwd><kwd>PGC-1α</kwd><kwd>oxidative stress</kwd><kwd>mitophagy</kwd><kwd>mitochondrial permeability transition pore</kwd><kwd>neuroprotection</kwd></kwd-group></article-meta></front><back><ref-list><title>References</title><ref id="cit1"><label>1</label><citation-alternatives><mixed-citation xml:lang="ru">Калашникова Л.А., Филатов А.С., Древаль М.В. 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