<?xml version="1.0" encoding="UTF-8"?>
<!DOCTYPE article PUBLIC "-//NLM//DTD JATS (Z39.96) Journal Publishing DTD v1.3 20210610//EN" "JATS-journalpublishing1-3.dtd">
<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">zabmedvestnik</journal-id><journal-title-group><journal-title xml:lang="ru">Забайкальский медицинский вестник</journal-title><trans-title-group xml:lang="en"><trans-title>Transbaikalian Medical Bulletin</trans-title></trans-title-group></journal-title-group><issn pub-type="epub">1998-6173</issn><publisher><publisher-name>Читинская государственная медицинская академия</publisher-name></publisher></journal-meta><article-meta><article-id pub-id-type="doi">10.52485/19986173_2024_1_139</article-id><article-id custom-type="elpub" pub-id-type="custom">zabmedvestnik-24</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>НАУЧНЫЕ ОБЗОРЫ</subject></subj-group><subj-group subj-group-type="section-heading" xml:lang="en"><subject>SCIENTIFIC REVIEWS</subject></subj-group></article-categories><title-group><article-title>РОЛЬ ОТДЕЛЬНЫХ МОЛЕКУЛ НЕЙРОВОСПАЛЕНИЯ В ПАТОГЕНЕЗЕ ИШЕМИЧЕСКОГО ИНСУЛЬТА. ЧАСТЬ I</article-title><trans-title-group xml:lang="en"><trans-title>THE ROLE OF INDIVIDUAL NEUROINFLAMMATION MOLECULES IN PATHOGENESIS ISCHEMIC STROKE. PART I</trans-title></trans-title-group></title-group><contrib-group><contrib contrib-type="author" corresp="yes"><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Ма-Ван-дэ</surname><given-names>А. Ю.</given-names></name><name name-style="western" xml:lang="en"><surname>Ma-Van-de</surname><given-names>А. Yu.</given-names></name></name-alternatives><bio xml:lang="ru"><p>672000, г. Чита., ул. Горького, 39А</p></bio><bio xml:lang="en"><p>39 A Gorkogo str., Chita, 672090</p></bio><xref ref-type="aff" rid="aff-1"/></contrib><contrib contrib-type="author" corresp="yes"><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Фефелова</surname><given-names>Е. В.</given-names></name><name name-style="western" xml:lang="en"><surname>Fefelova</surname><given-names>Е. V.</given-names></name></name-alternatives><bio xml:lang="ru"><p>672000, г. Чита., ул. Горького, 39А</p></bio><bio xml:lang="en"><p>39 A Gorkogo str., Chita, 672090</p></bio><xref ref-type="aff" rid="aff-1"/></contrib><contrib contrib-type="author" corresp="yes"><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Ширшов</surname><given-names>Ю. А.</given-names></name><name name-style="western" xml:lang="en"><surname>Shirshov</surname><given-names>Yu. A.</given-names></name></name-alternatives><bio xml:lang="ru"><p>672000, г. Чита., ул. Горького, 39А</p></bio><bio xml:lang="en"><p>39 A Gorkogo str., Chita, 672090</p></bio><xref ref-type="aff" rid="aff-1"/></contrib></contrib-group><aff-alternatives id="aff-1"><aff xml:lang="ru"><institution>Федеральное государственное бюджетное образовательное учреждение высшего образования «Читинская государственная медицинская академия» Министерства здравоохранения&#13;
Российской Федерации</institution><country>Россия</country></aff><aff xml:lang="en"><institution>Chita State Medical Academy</institution><country>Russian Federation</country></aff></aff-alternatives><pub-date pub-type="collection"><year>2024</year></pub-date><pub-date pub-type="epub"><day>18</day><month>05</month><year>2024</year></pub-date><volume>0</volume><issue>1</issue><fpage>139</fpage><lpage>147</lpage><permissions><copyright-statement>Copyright &amp;#x00A9; Ма-Ван-дэ А.Ю., Фефелова Е.В., Ширшов Ю.А., 2024</copyright-statement><copyright-year>2024</copyright-year><copyright-holder xml:lang="ru">Ма-Ван-дэ А.Ю., Фефелова Е.В., Ширшов Ю.А.</copyright-holder><copyright-holder xml:lang="en">Ma-Van-de А.Y., Fefelova Е.V., Shirshov Y.A.</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://www.zabmedvestnik.ru/jour/article/view/24">https://www.zabmedvestnik.ru/jour/article/view/24</self-uri><abstract><p>Ишемический инсульт – это острая, тяжёлая сосудистая патология головного мозга, сопровождающаяся общемозговой и очаговой неврологической симптоматикой. В основе возникновения заболевания лежит артериальный тромбоз, приводящий к образованию очага инфаркта мозговой ткани. В большинстве случаев после перенесенной острой церебральной катастрофы сохраняется стойкий неврологический дефицит в виде двигательных, когнитивных и других расстройств. Церебральный инфаркт является мультифакториальным заболеванием со сложным мультикаскадным патогенезом. Тяжесть течения заболевания, скорость восстановления пациентов и исход не всегда коррелируют с их возрастом, наличием фоновой и сопутствующей патологии. Поэтому в данный момент определённый интерес вызывает углубленное изучение патологических процессов, которые протекают непосредственно в очаге инфаркта мозга и в зоне пенумбры (ишемической полутени). Возможно, что более детальное понимание происходящих патологических процессов позволит в дальнейшем добиться более значимых результатов в процессе лечения и восстановления больных.</p><p>В представленном обзоре литературы освещены актуальные данные по основным патологическим процессам, которые протекают при ишемическом инсульте. Рассматривается роль микроглии как основного регулятора процессов воспаления, иммуносупрессии, дегенерации и репарации нервной ткани.</p></abstract><trans-abstract xml:lang="en"><p>Ischemic stroke is an acute, severe vascular pathology of the brain, accompanied by general cerebral and focal neurological symptoms. The occurrence of the disease is based on arterial thrombosis, leading to the formation of a focus of infarction of brain tissue. In most cases, after an acute cerebral accident, persistent neurological deficits persist in the form of motor, cognitive and other disorders. Cerebral infarction is a multifactorial disease with a complex multicascade pathogenesis. The severity of the disease, the speed of patient recovery and outcome do not always correlate with their age and the presence of underlying pathology. Therefore, at the moment, there is a certain interest in an in-depth study of the pathological processes that occur directly at the site of cerebral infarction and in the penumbra zone (ischemic penumbra). It is possible that a more detailed understanding of the ongoing pathological processes will allow us to further achieve better results in the process of treatment and recovery of patients.</p><p>The presented literature review highlights current data on the main pathological processes that occur during ischemic stroke. The role of microglia as the main regulator of the processes of inflammation, immunosuppression, degeneration and repair of nervous tissue is considered.</p></trans-abstract><kwd-group xml:lang="ru"><kwd>цереброваскулярные заболевания</kwd><kwd>острое нарушение мозгового кровообращения (ОНМК)</kwd><kwd>ишемический инсульт</kwd><kwd>микроглия</kwd><kwd>нейровоспаление</kwd><kwd>нейродегенерация</kwd></kwd-group><kwd-group xml:lang="en"><kwd>cerebrovascular diseases</kwd><kwd>acute cerebrovascular accident</kwd><kwd>ischemic stroke</kwd><kwd>microglia</kwd><kwd>neuroinflammation</kwd><kwd>neurodegeneration</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">Roth G., Abate D., Abate K. H., Abay S. M., Abbafati C., et. al. Global, regional, and national age-sexspecific mortality for 282 causes of death in 195 countries and territories, 1980- 2017: a systematic analysis for the Global Burden of Disease Study 2017. The Lancet. 2018. 10 (392). 1736-1788.</mixed-citation><mixed-citation xml:lang="en">Roth G., Abate D., Abate K.H., Abay S.M., Abbafati C., et. al. Global, regional, and national age-sexspecific mortality for 282 causes of death in 195 countries and territories, 1980- 2017: a systematic analysis for the Global Burden of Disease Study 2017. The Lancet. 2018. 10 (392). 1736-1788.</mixed-citation></citation-alternatives></ref><ref id="cit2"><label>2</label><citation-alternatives><mixed-citation xml:lang="ru">Котова Е.Г., Кобыкова О.С., Стародубов В.И., Александрова Г.А., Голубев Н.А., и др. Заболеваемость всего населения России в 2022 году с диагнозом, установленным впервые в жизни: статистические материалы. М.: ФГБУ «Центральный научно-исследовательский институт организации и информатизации здравоохранения» Минздрава России. 2023. 81-83.</mixed-citation><mixed-citation xml:lang="en">Kotova E.G., Kobykova O.S., Starodubov V.I., Aleksandrova G.A., Golubev N.A., et al. Morbidity of the entire population of Russia in 2022 with a diagnosis established for the first time in life: statistical materials. M.: Federal State Budgetary Institution " Central Research Institute for Organization and Informatization of Health Care" of the Ministry of Health of Russia. 2023. 81-83.</mixed-citation></citation-alternatives></ref><ref id="cit3"><label>3</label><citation-alternatives><mixed-citation xml:lang="ru">Гусев Е.И., Коновалов А.Н., Скворцова В.И. Неврология. Национальное руководство. г. Москва «ГЭОТАР-Медиа», 2022. 1. 298-300.</mixed-citation><mixed-citation xml:lang="en">Gusev E.I., Konovalov A.N., Skvortsova V.I. Neurology. National leadership. Moscow "GEOTAR-Media", 2022. 1. 298-300.</mixed-citation></citation-alternatives></ref><ref id="cit4"><label>4</label><citation-alternatives><mixed-citation xml:lang="ru">Khoshnam S.E., Winlow W., Farzaneh M., Farbood Y., Moghaddam H.F. Pathogenic mechanisms following ischemic stroke. Neurological Sciences. 2017. 38. 1167-1186.</mixed-citation><mixed-citation xml:lang="en">Khoshnam S.E., Winlow W., Farzaneh M., Farbood Y., Moghaddam H.F. Pathogenic mechanisms following ischemic stroke. Neurological Sciences. 2017. 38. 1167-1186.</mixed-citation></citation-alternatives></ref><ref id="cit5"><label>5</label><citation-alternatives><mixed-citation xml:lang="ru">Guo J.D., Zhao X., Li Y., Li G.R., Liu X.L. Damage to dopaminergic neurons by oxidative stress in Parkinson's disease (Review). International Journal of Molecular Medicine. 2018. 41. 1817-1825.</mixed-citation><mixed-citation xml:lang="en">Guo J.D., Zhao X., Li Y., Li G.R., Liu X.L. Damage to dopaminergic neurons by oxidative stress in Parkinson's disease (Review). International Journal of Molecular Medicine. 2018. 41. 1817-1825.</mixed-citation></citation-alternatives></ref><ref id="cit6"><label>6</label><citation-alternatives><mixed-citation xml:lang="ru">Endres M., Moro M.A., Nolte C.H., Dames C., Buckwalter M.S., Meisel A. Immune pathways in etiology, acute phase, and chronic sequelae of ischemic stroke. Circulation Research. 2022. 130 (8). 1167-1186.</mixed-citation><mixed-citation xml:lang="en">Endres M., Moro M.A., Nolte C.H., Dames C., Buckwalter M.S., Meisel A. Immune pathways in etiology, acute phase, and chronic sequelae of ischemic stroke. Circulation Research. 2022. 130 (8). 1167-1186.</mixed-citation></citation-alternatives></ref><ref id="cit7"><label>7</label><citation-alternatives><mixed-citation xml:lang="ru">Di Napoli M., Elkind M.S., Godoy D.A., Singh P., Papa F., et. al. Role of c-reactive protein in cerebrovascular disease: a critical review. Expert Review of Cardiovascular Therapy. 2011. 9 (12). 1565- 1584.</mixed-citation><mixed-citation xml:lang="en">Di Napoli M., Elkind M.S., Godoy D.A., Singh P., Papa F., et. al. Role of c-reactive protein in cerebrovascular disease: a critical review. Expert Review of Cardiovascular Therapy. 2011. 9(12). 1565- 1584.</mixed-citation></citation-alternatives></ref><ref id="cit8"><label>8</label><citation-alternatives><mixed-citation xml:lang="ru">Liu R., Song P., Gu X., Liang W., Sun W., et al. Comprehensive landscape of immune infiltration and aberrant pathway activation in ischemic stroke. Frontiers in Immunology. 2022. 12. 766724.</mixed-citation><mixed-citation xml:lang="en">Liu R., Song P., Gu X., Liang W., Sun W., et al. Comprehensive landscape of immune infiltration and aberrant pathway activation in ischemic stroke. Frontiers in Immunology. 2022. 12. 766724.</mixed-citation></citation-alternatives></ref><ref id="cit9"><label>9</label><citation-alternatives><mixed-citation xml:lang="ru">Rana A.K., Singh D. Targeting glycogen synthase kinase-3 for oxidative stress and neuroinflammation: Opportunities, challenges and future directions for cerebral stroke management. Neuropharmacology. 2018. 139. 124-136.</mixed-citation><mixed-citation xml:lang="en">Rana A.K., Singh D. Targeting glycogen synthase kinase-3 for oxidative stress and neuroinflammation: Opportunities, challenges and future directions for cerebral stroke management. Neuropharmacology. 2018. 139. 124-136.</mixed-citation></citation-alternatives></ref><ref id="cit10"><label>10</label><citation-alternatives><mixed-citation xml:lang="ru">Prinz M., Masuda T., Wheeler M.A., Quintana F.J. Microglia and Central Nervous System-Associated Macrophages-From Origin to Disease Modulation. Annual Review of Immunology. 2021. 39. 251-277.</mixed-citation><mixed-citation xml:lang="en">Prinz M., Masuda T., Wheeler M.A., Quintana F.J. Microglia and Central Nervous System-Associated Macrophages-From Origin to Disease Modulation. Annual Review of Immunology. 2021. 39. 251-277.</mixed-citation></citation-alternatives></ref><ref id="cit11"><label>11</label><citation-alternatives><mixed-citation xml:lang="ru">Goldmann T., Wieghofer P., Jordão M.J.C., Prutek F., Hagemeyer N., et al. Origin, fate and dynamics of macrophages at central nervous system interfaces. Nature Immunology. 2016. 17. 797-805.</mixed-citation><mixed-citation xml:lang="en">Goldmann T., Wieghofer P., Jordão M.J.C., Prutek F., Hagemeyer N., et al. Origin, fate and dynamics of macrophages at central nervous system interfaces. Nature Immunology. 2016. 17. 797-805.</mixed-citation></citation-alternatives></ref><ref id="cit12"><label>12</label><citation-alternatives><mixed-citation xml:lang="ru">Ginhoux F., Garel S. The mysterious origins of microglia. Nature Neuroscience. 2018. 21. 897-899.</mixed-citation><mixed-citation xml:lang="en">Ginhoux F., Garel S. The mysterious origins of microglia. Nature Neuroscience. 2018. 21. 897-899.</mixed-citation></citation-alternatives></ref><ref id="cit13"><label>13</label><citation-alternatives><mixed-citation xml:lang="ru">Spittau B., Dokalis N., Prinz M. The Role of TGFβ Signaling in Microglia Maturation and Activation. Trends in Immunology. 2020. 41 (9). 836-848.</mixed-citation><mixed-citation xml:lang="en">Spittau B., Dokalis N., Prinz M. The Role of TGFβ Signaling in Microglia Maturation and Activation. Trends in Immunology. 2020. 41 (9). 836-848.</mixed-citation></citation-alternatives></ref><ref id="cit14"><label>14</label><citation-alternatives><mixed-citation xml:lang="ru">Xiang C., Li H., Tang W. Targeting CSF-1R represents an effective strategy in modulating inflammatory diseases. Pharmacological Research. 2023. 187. 106566.</mixed-citation><mixed-citation xml:lang="en">Xiang C., Li H., Tang W. Targeting CSF-1R represents an effective strategy in modulating inflammatory diseases. Pharmacological Research. 2023. 187. 106566.</mixed-citation></citation-alternatives></ref><ref id="cit15"><label>15</label><citation-alternatives><mixed-citation xml:lang="ru">Percin G. I. CSF1R regulates the dendritic cell pool size in adult mice via embryo-derived tissue-resident macrophages. Nature Communications. 2018. 9. 1-12.</mixed-citation><mixed-citation xml:lang="en">Percin G. I. CSF1R regulates the dendritic cell pool size in adult mice via embryo-derived tissue-resident macrophages. Nature Communications. 2018. 9. 1-12.</mixed-citation></citation-alternatives></ref><ref id="cit16"><label>16</label><citation-alternatives><mixed-citation xml:lang="ru">Su C., Miao J., Guo J. The relationship between TGF-β1 and cognitive function in the brain. Brain Research Bulletin. 2023. 205. 110820.</mixed-citation><mixed-citation xml:lang="en">Su C., Miao J., Guo J. The relationship between TGF-β1 and cognitive function in the brain. Brain Research Bulletin. 2023. 205. 110820.</mixed-citation></citation-alternatives></ref><ref id="cit17"><label>17</label><citation-alternatives><mixed-citation xml:lang="ru">Feng X., Feng W., Ji Y., Jin T., Li J., et. al. Transforming growth factor-beta1 negatively regulates SOCS7 via EGR1 during wound healing. Cell Communication and Signaling. 2022. 20.</mixed-citation><mixed-citation xml:lang="en">Feng X., Feng W., Ji Y., Jin T., Li J., et. al. Transforming growth factor-beta1 negatively regulates SOCS7 via EGR1 during wound healing. Cell Communication and Signaling. 2022. 20.</mixed-citation></citation-alternatives></ref><ref id="cit18"><label>18</label><citation-alternatives><mixed-citation xml:lang="ru">Lodyga M., Hinz B. TGF-beta1 - A truly transforming growth factor in fibrosis and immunity. Seminars in Cell and Developmental Biology. 2020. 101. 123-139.</mixed-citation><mixed-citation xml:lang="en">Lodyga M., Hinz B. TGF-beta1 - A truly transforming growth factor in fibrosis and immunity. Seminars in Cell and Developmental Biology. 2020. 101. 123-139.</mixed-citation></citation-alternatives></ref><ref id="cit19"><label>19</label><citation-alternatives><mixed-citation xml:lang="ru">Meng X.M., Nikolic-Paterson D.J., Lan H.Y. TGF-beta: the master regulator of fibrosis. Nature Reviews Nephrology. 2016. 12. 325-338.</mixed-citation><mixed-citation xml:lang="en">Meng X.M., Nikolic-Paterson D.J., Lan H.Y. TGF-beta: the master regulator of fibrosis. Nature Reviews Nephrology. 2016. 12. 325-338.</mixed-citation></citation-alternatives></ref><ref id="cit20"><label>20</label><citation-alternatives><mixed-citation xml:lang="ru">Gibon J., Barker P. A. Neurotrophins and proneurotrophins: focus on synaptic activity and plasticity in the brain. The Neuroscientist. 2017. 23 (6). 587-604.</mixed-citation><mixed-citation xml:lang="en">Gibon J., Barker P.A. Neurotrophins and proneurotrophins: focus on synaptic activity and plasticity in the brain. The Neuroscientist. 2017. 23 (6). 587-604.</mixed-citation></citation-alternatives></ref><ref id="cit21"><label>21</label><citation-alternatives><mixed-citation xml:lang="ru">Liu D., Flory J., Lin A. Characterization of on-target adverse events caused by TRK inhibitor therapy. Annals of Oncology. 2020. 31 (9). 1207-1215.</mixed-citation><mixed-citation xml:lang="en">Liu D., Flory J., Lin A. Characterization of on-target adverse events caused by TRK inhibitor therapy. Annals of Oncology. 2020. 31(9). 1207-1215.</mixed-citation></citation-alternatives></ref><ref id="cit22"><label>22</label><citation-alternatives><mixed-citation xml:lang="ru">Sims S.K., Wilken-Resman B., Smith C.J., Mitchell A., McGonegal L., Sims-Robinson C. Brain-Derived Neurotrophic Factor and Nerve Growth Factor Therapeutics for Brain Injury: The Current Translational Challenges in Preclinical and Clinical Research. Neural Plasticity. 2022. 3889300.</mixed-citation><mixed-citation xml:lang="en">Sims S.K., Wilken-Resman B., Smith C.J., Mitchell A., McGonegal L., Sims-Robinson C. Brain-Derived Neurotrophic Factor and Nerve Growth Factor Therapeutics for Brain Injury: The Current Translational Challenges in Preclinical and Clinical Research. Neural Plasticity. 2022. 3889300.</mixed-citation></citation-alternatives></ref><ref id="cit23"><label>23</label><citation-alternatives><mixed-citation xml:lang="ru">De Camilli P., Cameron R., Greengard P. Synapsin I (protein I), a nerve terminal-specific phosphoprotein. I. Its general distribution in synapses of the central and peripheral nervous system demonstrated by immunofluorescence in frozen and plastic sections. Journal of Cell Biology. 1983. 96 (5). 1337-1354.</mixed-citation><mixed-citation xml:lang="en">De Camilli P., Cameron R., Greengard P. Synapsin I (protein I), a nerve terminal-specific phosphoprotein. I. Its general distribution in synapses of the central and peripheral nervous system demonstrated by immunofluorescence in frozen and plastic sections. Journal of Cell Biology. 1983. 96 (5). 1337-1354.</mixed-citation></citation-alternatives></ref><ref id="cit24"><label>24</label><citation-alternatives><mixed-citation xml:lang="ru">Cesca F., Baldelli P., Valtorta F., Benfenati F. The synapsins: key actors of synapse function and plasticity. Progress in Neurobiology. 2010. 91. 313-348.</mixed-citation><mixed-citation xml:lang="en">Cesca F., Baldelli P., Valtorta F., Benfenati F. The synapsins: key actors of synapse function and plasticity. Progress in Neurobiology. 2010. 91. 313-348.</mixed-citation></citation-alternatives></ref><ref id="cit25"><label>25</label><citation-alternatives><mixed-citation xml:lang="ru">Galasko D., Xiao M., Xu D., Smirnov D., Salmon D.P., et al. Alzheimer's Disease Neuroimaging Initiative (ADNI); Worley P. Synaptic biomarkers in CSF aid in diagnosis, correlate with cognition and predict progression in MCI and Alzheimer's disease. Alzheimer's &amp; Dementia Journal. 2019. 12 (5). 871-882.</mixed-citation><mixed-citation xml:lang="en">Galasko D., Xiao M., Xu D., Smirnov D., Salmon D.P., et al. Alzheimer's Disease Neuroimaging Initiative (ADNI); Worley P. Synaptic biomarkers in CSF aid in diagnosis, correlate with cognition and predict progression in MCI and Alzheimer's disease. Alzheimer's &amp; Dementia Journal. 2019. 12 (5). 871-882.</mixed-citation></citation-alternatives></ref><ref id="cit26"><label>26</label><citation-alternatives><mixed-citation xml:lang="ru">Halbgebauer S., Steinacker P., Riedel D., Oeckl P., Anderl-Straub S., et al. Visinin-like protein 1 levels in blood and CSF as emerging markers for Alzheimer's and other neurodegenerative diseases. Alzheimer's Research &amp; Therapy. 2022. 11 (1).</mixed-citation><mixed-citation xml:lang="en">Halbgebauer S., Steinacker P., Riedel D., Oeckl P., Anderl-Straub S., et al. Visinin-like protein 1 levels in blood and CSF as emerging markers for Alzheimer's and other neurodegenerative diseases. Alzheimer's Research &amp; Therapy. 2022. 11 (1).</mixed-citation></citation-alternatives></ref><ref id="cit27"><label>27</label><citation-alternatives><mixed-citation xml:lang="ru">Li Y., Wu X-Q., Fan Q, et al. A study on the correlation of cognitive dysfunction after stroke with the levels of vilip-1 and hs-crp in serum. Acta Medica Mediterranea. 2018. 34. 1895-1899.</mixed-citation><mixed-citation xml:lang="en">Li Y., Wu X-Q., Fan Q, et al. A study on the correlation of cognitive dysfunction after stroke with the levels of vilip-1 and hs-crp in serum. Acta Medica Mediterranea. 2018. 34. 1895-1899.</mixed-citation></citation-alternatives></ref><ref id="cit28"><label>28</label><citation-alternatives><mixed-citation xml:lang="ru">Liu D., Dong X., Yang R., Guo H., Wang T., et. al. Visinin-like protein-1 level is associated with short-term functional outcome of acute ischemic stroke: A prospective cohort study. Medicine (Baltimore). 2020. 99 (9).</mixed-citation><mixed-citation xml:lang="en">Liu D., Dong X., Yang R., Guo H., Wang T., et. al. Visinin-like protein-1 level is associated with shortterm functional outcome of acute ischemic stroke: A prospective cohort study. Medicine (Baltimore). 2020. 99 (9).</mixed-citation></citation-alternatives></ref><ref id="cit29"><label>29</label><citation-alternatives><mixed-citation xml:lang="ru">Shibuya M. Vascular Endothelial Growth Factor (VEGF) and Its Receptor (VEGFR) Signaling in Angiogenesis: A Crucial Target for Anti- and Pro-Angiogenic Therapies. Genes Cancer. 2011. 12 (12). 1097-1105.</mixed-citation><mixed-citation xml:lang="en">Shibuya M. Vascular Endothelial Growth Factor (VEGF) and Its Receptor (VEGFR) Signaling in Angiogenesis: A Crucial Target for Anti- and Pro-Angiogenic Therapies. Genes Cancer. 2011. 12 (12). 1097-1105.</mixed-citation></citation-alternatives></ref><ref id="cit30"><label>30</label><citation-alternatives><mixed-citation xml:lang="ru">Holmes D.I., Zachary, I. The vascular endothelial growth factor (VEGF) family: Angiogenic factors in health and disease. Genome Biology. 2005. 6.</mixed-citation><mixed-citation xml:lang="en">Holmes D.I., Zachary, I. The vascular endothelial growth factor (VEGF) family: Angiogenic factors in health and disease. Genome Biology. 2005. 6.</mixed-citation></citation-alternatives></ref><ref id="cit31"><label>31</label><citation-alternatives><mixed-citation xml:lang="ru">Issa R., Krupinski J., Bujny T., Kumar S., Kaluza J., et. al. Vascular endothelial growth factor and its receptor, KDR, in human brain tissue after ischemic stroke. Laboratory Investigation. 1999. 7 (4). 417-425.</mixed-citation><mixed-citation xml:lang="en">Issa R., Krupinski J., Bujny T., Kumar S., Kaluza J., et. al. Vascular endothelial growth factor and its receptor, KDR, in human brain tissue after ischemic stroke. Laboratory Investigation. 1999. 7 (4). 417-425.</mixed-citation></citation-alternatives></ref><ref id="cit32"><label>32</label><citation-alternatives><mixed-citation xml:lang="ru">Moon S., Chang M.S., Koh S.H., Choi Y.K. Repair Mechanisms of the Neurovascular Unit after Ischemic Stroke with a Focus on VEGF. International Journal of Molecular Sciences. 2021. 8 (16).</mixed-citation><mixed-citation xml:lang="en">Moon S., Chang M.S., Koh S.H., Choi Y.K. Repair Mechanisms of the Neurovascular Unit after Ischemic Stroke with a Focus on VEGF. International Journal of Molecular Sciences. 2021. 8 (16).</mixed-citation></citation-alternatives></ref><ref id="cit33"><label>33</label><citation-alternatives><mixed-citation xml:lang="ru">Colonna M. The biology of TREM receptors. Nature Reviews Immunology. 2023. 23 (9). 580-594.</mixed-citation><mixed-citation xml:lang="en">Colonna M. The biology of TREM receptors. Nature Reviews Immunology. 2023. 23 (9). 580-594.</mixed-citation></citation-alternatives></ref><ref id="cit34"><label>34</label><citation-alternatives><mixed-citation xml:lang="ru">Lu Q., Liu R., Sherchan P. et al. TREM (triggering receptor expressed on myeloid cells)-1 inhibition attenuates neuroinflammation via PKC (protein kinase C) delta/CARD9 (caspase recruitment domain family member 9) signaling pathway after intracerebral hemorrhage in mice. Stroke. 2021. 52. 2162-2173</mixed-citation><mixed-citation xml:lang="en">Lu Q., Liu R., Sherchan P. et al. TREM (triggering receptor expressed on myeloid cells)-1 inhibition attenuates neuroinflammation via PKC (protein kinase C) delta/CARD9 (caspase recruitment domain family member 9) signaling pathway after intracerebral hemorrhage in mice. Stroke. 2021. 52. 2162-2173</mixed-citation></citation-alternatives></ref><ref id="cit35"><label>35</label><citation-alternatives><mixed-citation xml:lang="ru">Lu L., Liu X., Fu J., Liang J., Hou Y., et. al. sTREM-1 promotes the phagocytic function of microglia to induce hippocampus damage via the PI3K-AKT signaling pathway. Scientific Reports. 2022. 12 (1).</mixed-citation><mixed-citation xml:lang="en">Lu L., Liu X., Fu J., Liang J., Hou Y., et. al. sTREM-1 promotes the phagocytic function of microglia to induce hippocampus damage via the PI3K-AKT signaling pathway. Scientific Reports. 2022. 12 (1).</mixed-citation></citation-alternatives></ref><ref id="cit36"><label>36</label><citation-alternatives><mixed-citation xml:lang="ru">Feng C.W. Chen N.F. Sung C.S. et al. Therapeutic effect of modulating TREM-1 via anti-inflammation and autophagy in Parkinson's disease. Frontiers in Neuroscience. 2019. 13.</mixed-citation><mixed-citation xml:lang="en">Feng C.W. Chen N.F. Sung C.S. et al. Therapeutic effect of modulating TREM-1 via anti-inflammation and autophagy in Parkinson's disease. Frontiers in Neuroscience. 2019. 13.</mixed-citation></citation-alternatives></ref><ref id="cit37"><label>37</label><citation-alternatives><mixed-citation xml:lang="ru">Kluckova K., Kozak J., Szaboova K., et al. TREM-1 and TREM-2 expression on blood monocytes could help predict survival in high-grade glioma patients. Mediators of Inflammation. 2020. 20201798147.</mixed-citation><mixed-citation xml:lang="en">Kluckova K., Kozak J., Szaboova K., et al. TREM-1 and TREM-2 expression on blood monocytes could help predict survival in high-grade glioma patients. Mediators of Inflammation. 2020. 20201798147.</mixed-citation></citation-alternatives></ref><ref id="cit38"><label>38</label><citation-alternatives><mixed-citation xml:lang="ru">Fan L., Liu Y., Wang Z., Mei X. Prognostic utility of sTREM-1 in predicting early neurological deterioration in patients with acute ischemic stroke treated without reperfusion therapy. Journal of Stroke &amp; Cerebrovascular Diseases. 2023. 32 (11). 107381.</mixed-citation><mixed-citation xml:lang="en">Fan L., Liu Y., Wang Z., Mei X. Prognostic utility of sTREM-1 in predicting early neurological deterioration in patients with acute ischemic stroke treated without reperfusion therapy. Journal of Stroke &amp; Cerebrovascular Diseases. 2023. 32 (11). 107381.</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>
