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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">sredob</journal-id><journal-title-group><journal-title xml:lang="ru">Здоровье населения и среда обитания – ЗНиСО</journal-title><trans-title-group xml:lang="en"><trans-title>Public Health and Life Environment – PH&amp;LE</trans-title></trans-title-group></journal-title-group><issn pub-type="ppub">2219-5238</issn><issn pub-type="epub">2619-0788</issn><publisher><publisher-name>ФБУЗ ФЦГиЭ Роспотребнадзора</publisher-name></publisher></journal-meta><article-meta><article-id pub-id-type="doi">10.35627/2219-5238/2022-30-9-35-42</article-id><article-id custom-type="elpub" pub-id-type="custom">sredob-1155</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>МЕДИЦИНА ТРУДА</subject></subj-group><subj-group subj-group-type="section-heading" xml:lang="en"><subject>OCCUPATIONAL MEDICINE</subject></subj-group></article-categories><title-group><article-title>Метаболомное профилирование при атеросклеротическом поражении сосудов и влияние тяжелых металлов на протекание заболевания (обзор литературы)</article-title><trans-title-group xml:lang="en"><trans-title>Metabolomic Profiling in Atherosclerotic Lesions and the Effect of Heavy Metals on the Course of Disease: A Literature Review</trans-title></trans-title-group></title-group><contrib-group><contrib contrib-type="author" corresp="yes"><contrib-id contrib-id-type="orcid">https://orcid.org/0000-0002-5576-365X</contrib-id><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Унесихина</surname><given-names>М. С.</given-names></name><name name-style="western" xml:lang="en"><surname>Unesikhina</surname><given-names>M. S.</given-names></name></name-alternatives><bio xml:lang="ru"><p>Унесихина Мария Сергеевна – лаборант-исследователь отдела молекулярной биологии и электронной микроскопии</p><p>ул. Попова, д. 30, г. Екатеринбург, 620014</p></bio><bio xml:lang="en"><p>Maria S. Unesikhina, Laboratory Researcher, Department of Molecular Biology and Electron Microscopy</p><p>30 Popov Street, Yekaterinburg, 620014</p></bio><email xlink:type="simple">unesihinams@ymrc.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/0000-0001-6167-7347</contrib-id><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Чемезов</surname><given-names>А. И.</given-names></name><name name-style="western" xml:lang="en"><surname>Chemezov</surname><given-names>A. I.</given-names></name></name-alternatives><bio xml:lang="ru"><p>Чемезов Алексей Игоревич – научный сотрудник отдела молекулярной биологии и электронной микроскопии</p><p>ул. Попова, д. 30, г. Екатеринбург, 620014</p></bio><bio xml:lang="en"><p>Aleksei I. Chemezov, Researcher, Department of Molecular Biology and Electron Microscopy</p><p>30 Popov Street, Yekaterinburg, 620014</p></bio><email xlink:type="simple">chemezov198@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/0000-0002-1743-7642</contrib-id><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Сутункова</surname><given-names>М. П.</given-names></name><name name-style="western" xml:lang="en"><surname>Sutunkova</surname><given-names>M. P.</given-names></name></name-alternatives><bio xml:lang="ru"><p>Сутункова Марина Петровна – д.м.н., директор</p><p>ул. Попова, д. 30, г. Екатеринбург, 620014</p></bio><bio xml:lang="en"><p>Marina P. Sutunkova, Dr. Sci. (Med.), Director</p><p>30 Popov Street, Yekaterinburg, 620014</p></bio><email xlink:type="simple">sutunkova@ymrc.ru</email><xref ref-type="aff" rid="aff-1"/></contrib></contrib-group><aff-alternatives id="aff-1"><aff xml:lang="ru"><institution>ФБУН «Екатеринбургский медицинский-научный центр профилактики и охраны здоровья рабочих промпредприятий» Роспотребнадзора</institution><country>Россия</country></aff><aff xml:lang="en"><institution>Yekaterinburg Medical Research Center for Prophylaxis and Health Protection in Industrial Workers</institution><country>Russian Federation</country></aff></aff-alternatives><pub-date pub-type="collection"><year>2022</year></pub-date><pub-date pub-type="epub"><day>04</day><month>10</month><year>2022</year></pub-date><volume>0</volume><issue>9</issue><fpage>35</fpage><lpage>42</lpage><permissions><copyright-statement>Copyright &amp;#x00A9; Унесихина М.С., Чемезов А.И., Сутункова М.П., 2022</copyright-statement><copyright-year>2022</copyright-year><copyright-holder xml:lang="ru">Унесихина М.С., Чемезов А.И., Сутункова М.П.</copyright-holder><copyright-holder xml:lang="en">Unesikhina M.S., Chemezov A.I., Sutunkova M.P.</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://zniso.fcgie.ru/jour/article/view/1155">https://zniso.fcgie.ru/jour/article/view/1155</self-uri><abstract><p>Введение. На развитых металлургических предприятиях зачастую наблюдается превышение предельно допустимых концентраций тяжелых металлов, оказывающих пагубное влияние на здоровье рабочих. Тяжелые металлы вызывают окислительный стресс, являющийся одним из ключевых факторов развития атеросклеротического поражения сосудов. Атеросклероз приводит к сердечным приступам и инсультам, которые являются причиной гибели людей в 85 % случаев смерти от сердечно-сосудистых заболеваний.Цель: Изучение молекулярных механизмов атеросклероза сосудов и влияния тяжелых металлов на протекание заболевания.Методы. Использованы информационно-аналитические методы на основе обобщения и анализа современных научных исследований, опубликованных в реферативных базах данных NLM, Scopus, CyberLeninka, Google Scholar, eLibrary, а также в информационных порталах по состоянию на январь 2022 г. Отбор статей осуществлялся по принципу наличия в них сведений о патогенезе и влиянии тяжелых металлов на протекание атеросклероза. Было проанализировано более 400 статей, в результате их них отобрано 66 полнотекстовых материалов.Результаты. Показана связь между молекулярными механизмами атеросклероза и тяжелыми металлами, сопоставлены основные этапы развития заболевания и метаболомный профиль крови при патологии.Заключение. Представленный обзор литературы выявил проблемы в нормативной базе и практическом осуществлении гигиенической оценки влияния тяжелых металлов на протекание атеросклеротического поражения сосудов, одной из которых является недостаточная оценка вклада тяжелых металлов в протекание заболевания. На данный момент удалось обнаружить влияние тяжелых металлов лишь на изолированные процессы патогенеза атеросклероза: изменение проницаемости и разрушение сосудистых мембран, повышение окислительного стресса, воспаление, пролиферацию гладкомышечных клеток, изменение реологических свойств крови, повышенный риск тромбообразования. Найденные закономерности в изменении концентрации некоторых метаболитов крови и потенциальное пагубное влияние тяжелых металлов на поражение сосудов позволят в будущем разработать новые способы выявления атеросклероза и включить рабочих промышленных предприятий в группу риска для ранней диагностики заболевания.</p></abstract><trans-abstract xml:lang="en"><p>Introduction: In the developed metallurgical industry, maximum permissible concentrations of heavy metals in the work environment are often exceeded, and the elevated exposure levels have a detrimental effect on workers’ health. Heavy metals cause oxidative stress, which is key factor in the development of atherosclerotic lesions. Atherosclerosis, in its turn, is the primary cause of heart attacks and stroke, which account for 85 % of all deaths from cardiovascular diseases.Objective: To study molecular mechanisms of atherosclerosis and the impact of heavy metals on the disease course.Methods: We applied methods of information analysis based on the review and generalization of published up-to-date research data on the pathogenesis and effects of heavy metals on the course of atherosclerosis found in NLM, Scopus, Cyber- Leninka, Google Scholar, and eLibrary abstract and citation databases, as well as on information portals, as of January 2022. More than 400 papers were analyzed and 66 full-text articles were found eligible for inclusion in this review.Results: We established the relationship between the exposure to heavy metals and the molecular mechanisms of atherosclerosis and compared the main stages of the disease development with the respective blood metabolomic profiles.Conclusions: Our literature review has revealed problems in the regulatory framework and practical assessment of the contribution of heavy metal exposures to the course of atherosclerotic lesions. So far, the effect of heavy metals only on isolated processes of the pathogenesis of atherosclerosis has been established, such as a change in permeability and destruction of vascular membranes, increased oxidative stress, inflammation, proliferation of smooth muscle cells, changes in blood rheological properties, and an increased risk of thrombosis. The observed patterns in the change in concentrations of some blood metabolites and the potential adverse vascular effect of heavy metals will help develop new methods for detecting atherosclerosis and include industrial workers in the group at risk of the disease for its early diagnosis.</p></trans-abstract><kwd-group xml:lang="ru"><kwd>обзор</kwd><kwd>атеросклероз</kwd><kwd>метаболиты атеросклероза</kwd><kwd>тяжелые металлы</kwd></kwd-group><kwd-group xml:lang="en"><kwd>review</kwd><kwd>atherosclerosis</kwd><kwd>metabolites</kwd><kwd>heavy metals</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">WHO. Cardiovascular diseases (CVDs). 11 June 2021. Accessed June 21, 2022. https://www.who.int/en/news-room/fact-sheets/detail/cardiovascular-diseases-(cvds)</mixed-citation><mixed-citation xml:lang="en">WHO. Cardiovascular diseases (CVDs). 11 June 2021. Accessed June 21, 2022. https://www.who.int/en/news-room/fact-sheets/detail/cardiovascular-diseases-(cvds)</mixed-citation></citation-alternatives></ref><ref id="cit2"><label>2</label><citation-alternatives><mixed-citation xml:lang="ru">WHO. Who mortality database; 2022. Accessed June 21, 2022. https://platform.who.int/mortality/themes/theme-details/topics/topic-details/MDB/cardiovascular-diseases</mixed-citation><mixed-citation xml:lang="en">WHO. Who mortality database; 2022. Accessed June 21, 2022. https://platform.who.int/mortality/themes/theme-details/topics/topic-details/MDB/cardiovascular-diseases</mixed-citation></citation-alternatives></ref><ref id="cit3"><label>3</label><citation-alternatives><mixed-citation xml:lang="ru">Зубков В.А., Тришевская А.В., Малкова Е.А., Михеева Е.В. Содержание тяжелых металлов в почвах промышленных городов Свердловской области. Colloquium-journal. 2019. № 17-7 (41). С. 16–23.</mixed-citation><mixed-citation xml:lang="en">Zubkov VA, Trishevskaya AV, Malkova EA, Mikheeva EV. The heavy metals content in the soils of Sverdlovsk region industrial cities. Colloquium-Journal. 2019;(17-7(41)):16-23. (In Russ.)</mixed-citation></citation-alternatives></ref><ref id="cit4"><label>4</label><citation-alternatives><mixed-citation xml:lang="ru">Weisskopf MG, Jain N, Nie H, et al. A prospective study of bone lead concentration and death from all causes, cardiovascular diseases, and cancer in the Department of Veterans Affairs Normative Aging Study. Circulation. 2009;120(12):1056-1064. doi: 10.1161/CIRCULATIONAHA.108.827121</mixed-citation><mixed-citation xml:lang="en">Weisskopf MG, Jain N, Nie H, et al. A prospective study of bone lead concentration and death from all causes, cardiovascular diseases, and cancer in the Department of Veterans Affairs Normative Aging Study. Circulation. 2009;120(12):1056-1064. doi: 10.1161/CIRCULATIONAHA.108.827121</mixed-citation></citation-alternatives></ref><ref id="cit5"><label>5</label><citation-alternatives><mixed-citation xml:lang="ru">Tellez-Plaza M, Guallar E, Howard BV, et al. Cadmium exposure and incident cardiovascular disease. Epidemiology. 2013;24(3):421-429. doi: 10.1097/EDE.0b013e31828b0631</mixed-citation><mixed-citation xml:lang="en">Tellez-Plaza M, Guallar E, Howard BV, et al. Cadmium exposure and incident cardiovascular disease. Epidemiology. 2013;24(3):421-429. doi: 10.1097/EDE.0b013e31828b0631</mixed-citation></citation-alternatives></ref><ref id="cit6"><label>6</label><citation-alternatives><mixed-citation xml:lang="ru">Бухтияров И.В., Измеров Н.Ф., Тихонов Г.И. и др. Условия труда как фактор повышения смертности в трудоспособном возрасте. Медицина труда и промышленная экология. 2017. № 8. С. 43–49.</mixed-citation><mixed-citation xml:lang="en">Bukhtiyarov IV, Izmerov NF, Tikhonova GI, et al. Work conditions as a risk factor mortality increase in able-bodied population. Meditsina Truda i Promyshlennaya Ekologiya. 2017;(8):43-49. (In Russ.)</mixed-citation></citation-alternatives></ref><ref id="cit7"><label>7</label><citation-alternatives><mixed-citation xml:lang="ru">Кольман Я., Рём К.-Г. Наглядная биохимия. М.: Лаборатория знаний, 2019. 509 с.</mixed-citation><mixed-citation xml:lang="en">Koolman J, Roehm KH. Color Atlas of Biochemistry. Transl. by Mosolova TP. 6th ed. Moscow: Laboratoriya Znaniy Publ.; 2018. (In Russ.)</mixed-citation></citation-alternatives></ref><ref id="cit8"><label>8</label><citation-alternatives><mixed-citation xml:lang="ru">Dursun N, Arifoglu C, Süer C, Keskinol L. Blood pressure relationship to nitric oxide, lipid peroxidation, renal function, and renal blood flow in rats exposed to low lead levels. Biol Trace Elem Res. 2005;104(2):141-149. doi: 10.1385/BTER:104:2:141</mixed-citation><mixed-citation xml:lang="en">Dursun N, Arifoglu C, Süer C, Keskinol L. Blood pressure relationship to nitric oxide, lipid peroxidation, renal function, and renal blood flow in rats exposed to low lead levels. Biol Trace Elem Res. 2005;104(2):141-149. doi: 10.1385/BTER:104:2:141</mixed-citation></citation-alternatives></ref><ref id="cit9"><label>9</label><citation-alternatives><mixed-citation xml:lang="ru">Oliveira TF, Batista PR, Leal MA, et al. Chronic cadmium exposure accelerates the development of atherosclerosis and induces vascular dysfunction in the aorta of ApoE-/- mice. Biol Trace Elem Res. 2019;187(1):163-171. doi: 10.1007/s12011-018-1359-1</mixed-citation><mixed-citation xml:lang="en">Oliveira TF, Batista PR, Leal MA, et al. Chronic cadmium exposure accelerates the development of atherosclerosis and induces vascular dysfunction in the aorta of ApoE-/- mice. Biol Trace Elem Res. 2019;187(1):163-171. doi: 10.1007/s12011-018-1359-1</mixed-citation></citation-alternatives></ref><ref id="cit10"><label>10</label><citation-alternatives><mixed-citation xml:lang="ru">Vinchi F, Porto G, Simmelbauer A, et al. Atherosclerosis is aggravated by iron overload and ameliorated by dietary and pharmacological iron restriction. Eur Heart J. 2020;41(28):2681-2695. doi: 10.1093/eurheartj/ehz112</mixed-citation><mixed-citation xml:lang="en">Vinchi F, Porto G, Simmelbauer A, et al. Atherosclerosis is aggravated by iron overload and ameliorated by dietary and pharmacological iron restriction. Eur Heart J. 2020;41(28):2681-2695. doi: 10.1093/eurheartj/ehz112</mixed-citation></citation-alternatives></ref><ref id="cit11"><label>11</label><citation-alternatives><mixed-citation xml:lang="ru">Jomova K, Valko M. Advances in metal-induced oxidative stress and human disease. Toxicology. 2011;283(2-3):65-87. doi: 10.1016/j.tox.2011.03.001</mixed-citation><mixed-citation xml:lang="en">Jomova K, Valko M. Advances in metal-induced oxidative stress and human disease. Toxicology. 2011;283(2-3):65-87. doi: 10.1016/j.tox.2011.03.001</mixed-citation></citation-alternatives></ref><ref id="cit12"><label>12</label><citation-alternatives><mixed-citation xml:lang="ru">Zmysłowski A, Szterk A. Current knowledge on the mechanism of atherosclerosis and pro-atherosclerotic properties of oxysterols. Lipids Health Dis. 2017;16(1):188. doi: 10.1186/s12944-017-0579-2</mixed-citation><mixed-citation xml:lang="en">Zmysłowski A, Szterk A. Current knowledge on the mechanism of atherosclerosis and pro-atherosclerotic properties of oxysterols. Lipids Health Dis. 2017;16(1):188. doi: 10.1186/s12944-017-0579-2</mixed-citation></citation-alternatives></ref><ref id="cit13"><label>13</label><citation-alternatives><mixed-citation xml:lang="ru">Bogomolova AM, Nikitin AA, Orlov SV, et al. Hypoxia as a factor involved in the regulation of the apoA-1, ABCA1, and complement C3 gene expression in human macrophages. Biochemistry (Mosc). 2019;84(5):529-539. doi: 10.1134/S0006297919050079</mixed-citation><mixed-citation xml:lang="en">Bogomolova AM, Nikitin AA, Orlov SV, et al. Hypoxia as a factor involved in the regulation of the apoA-1, ABCA1, and complement C3 gene expression in human macrophages. Biochemistry (Mosc). 2019;84(5):529-539. doi: 10.1134/S0006297919050079</mixed-citation></citation-alternatives></ref><ref id="cit14"><label>14</label><citation-alternatives><mixed-citation xml:lang="ru">Hultgardh-Nilsson A, Borén J, Chakravarti S. The small leucine-rich repeat proteoglycans in tissue repair and atherosclerosis. J Intern Med. 2015;278(5):447-461. doi: 10.1111/joim.12400</mixed-citation><mixed-citation xml:lang="en">Hultgardh-Nilsson A, Borén J, Chakravarti S. The small leucine-rich repeat proteoglycans in tissue repair and atherosclerosis. J Intern Med. 2015;278(5):447-461. doi: 10.1111/joim.12400</mixed-citation></citation-alternatives></ref><ref id="cit15"><label>15</label><citation-alternatives><mixed-citation xml:lang="ru">Devlin CM, Leventhal AR, Kuriakose G, Schuchman EH, Williams KJ, Tabas I. Acid sphingomyelinase promotes lipoprotein retention within early atheromata and accelerates lesion progression. Arterioscler Thromb Vasc Biol. 2008;28(10):1723-1730. doi: 10.1161/ATVBAHA.108.173344</mixed-citation><mixed-citation xml:lang="en">Devlin CM, Leventhal AR, Kuriakose G, Schuchman EH, Williams KJ, Tabas I. Acid sphingomyelinase promotes lipoprotein retention within early atheromata and accelerates lesion progression. Arterioscler Thromb Vasc Biol. 2008;28(10):1723-1730. doi: 10.1161/ATVBAHA.108.173344</mixed-citation></citation-alternatives></ref><ref id="cit16"><label>16</label><citation-alternatives><mixed-citation xml:lang="ru">Silverstein RL. Inflammation, atherosclerosis, and arterial thrombosis: role of the scavenger receptor CD36. Cleve Clin J Med. 2009;76(Suppl 2):S27-S30. doi: 10.3949/ccjm.76.s2.06</mixed-citation><mixed-citation xml:lang="en">Silverstein RL. Inflammation, atherosclerosis, and arterial thrombosis: role of the scavenger receptor CD36. Cleve Clin J Med. 2009;76(Suppl 2):S27-S30. doi: 10.3949/ccjm.76.s2.06</mixed-citation></citation-alternatives></ref><ref id="cit17"><label>17</label><citation-alternatives><mixed-citation xml:lang="ru">Jan AT, Azam M, Siddiqui K, Ali A, Choi I, Haq QM. Heavy metals and human health: Mechanistic insight into toxicity and counter defense system of antioxidants. Int J Mol Sci. 2015;16(12):29592-29630. doi: 10.3390/ijms161226183</mixed-citation><mixed-citation xml:lang="en">Jan AT, Azam M, Siddiqui K, Ali A, Choi I, Haq QM. Heavy metals and human health: Mechanistic insight into toxicity and counter defense system of antioxidants. Int J Mol Sci. 2015;16(12):29592-29630. doi: 10.3390/ijms161226183</mixed-citation></citation-alternatives></ref><ref id="cit18"><label>18</label><citation-alternatives><mixed-citation xml:lang="ru">Chen L, Liang B, Froese DE, et al. Oxidative modification of low density lipoprotein in normal and hyperlipidemic patients: effect of lysophosphatidylcholine composition on vascular relaxation. J Lipid Res. 1997;38(3):546-553.</mixed-citation><mixed-citation xml:lang="en">Chen L, Liang B, Froese DE, et al. Oxidative modification of low density lipoprotein in normal and hyperlipidemic patients: effect of lysophosphatidylcholine composition on vascular relaxation. J Lipid Res. 1997;38(3):546-553.</mixed-citation></citation-alternatives></ref><ref id="cit19"><label>19</label><citation-alternatives><mixed-citation xml:lang="ru">Zhang F, Jia Z, Gao P, et al. Metabonomics study of atherosclerosis rats by ultra fast liquid chromatography coupled with ion trap-time of flight mass spectrometry. Talanta. 2009;79(3):836-844. doi: 10.1016/j.talanta.2009.05.010</mixed-citation><mixed-citation xml:lang="en">Zhang F, Jia Z, Gao P, et al. Metabonomics study of atherosclerosis rats by ultra fast liquid chromatography coupled with ion trap-time of flight mass spectrometry. Talanta. 2009;79(3):836-844. doi: 10.1016/j.talanta.2009.05.010</mixed-citation></citation-alternatives></ref><ref id="cit20"><label>20</label><citation-alternatives><mixed-citation xml:lang="ru">Tomas L, Edsfeldt A, Mollet IG, et al. Altered metabolism distinguishes high-risk from stable carotid atherosclerotic plaques. Eur Heart J. 2018;39(24):2301-2310. doi: 10.1093/eurheartj/ehy124</mixed-citation><mixed-citation xml:lang="en">Tomas L, Edsfeldt A, Mollet IG, et al. Altered metabolism distinguishes high-risk from stable carotid atherosclerotic plaques. Eur Heart J. 2018;39(24):2301-2310. doi: 10.1093/eurheartj/ehy124</mixed-citation></citation-alternatives></ref><ref id="cit21"><label>21</label><citation-alternatives><mixed-citation xml:lang="ru">Liu YT, Peng JB, Jia HM, et al. UPLC-Q/TOF MS standardized Chinese formula Xin-Ke-Shu for the treatment of atherosclerosis in a rabbit model. Phytomedicine. 2014;21(11):1364-1372. doi: 10.1016/j.phymed.2014.05.009</mixed-citation><mixed-citation xml:lang="en">Liu YT, Peng JB, Jia HM, et al. UPLC-Q/TOF MS standardized Chinese formula Xin-Ke-Shu for the treatment of atherosclerosis in a rabbit model. Phytomedicine. 2014;21(11):1364-1372. doi: 10.1016/j.phymed.2014.05.009</mixed-citation></citation-alternatives></ref><ref id="cit22"><label>22</label><citation-alternatives><mixed-citation xml:lang="ru">Izidoro MA, Cecconi A, Panadero MI, et al. Plasma metabolic signature of atherosclerosis progression and colchicine treatment in rabbits. Sci Rep. 2020;10(1):7072. doi: 10.1038/s41598-020-63306-y</mixed-citation><mixed-citation xml:lang="en">Izidoro MA, Cecconi A, Panadero MI, et al. Plasma metabolic signature of atherosclerosis progression and colchicine treatment in rabbits. Sci Rep. 2020;10(1):7072. doi: 10.1038/s41598-020-63306-y</mixed-citation></citation-alternatives></ref><ref id="cit23"><label>23</label><citation-alternatives><mixed-citation xml:lang="ru">Stübiger G, Aldover-Macasaet E, Bicker W, et al. Targeted profiling of atherogenic phospholipids in human plasma and lipoproteins of hyperlipidemic patients using MALDI-QIT-TOF-MS/MS. Atherosclerosis. 2012;224(1):177-186. doi: 10.1016/j.atherosclerosis. 2012.06.010</mixed-citation><mixed-citation xml:lang="en">Stübiger G, Aldover-Macasaet E, Bicker W, et al. Targeted profiling of atherogenic phospholipids in human plasma and lipoproteins of hyperlipidemic patients using MALDI-QIT-TOF-MS/MS. Atherosclerosis. 2012;224(1):177-186. doi: 10.1016/j.atherosclerosis. 2012.06.010</mixed-citation></citation-alternatives></ref><ref id="cit24"><label>24</label><citation-alternatives><mixed-citation xml:lang="ru">Mazerik JN, Mikkilineni H, Kuppusamy VA, et al. Mercury activates phospholipase a(2) and induces formation of arachidonic acid metabolites in vascular endothelial cells. Toxicol Mech Methods. 2007;17(9):541-557. doi: 10.1080/15376510701380505</mixed-citation><mixed-citation xml:lang="en">Mazerik JN, Mikkilineni H, Kuppusamy VA, et al. Mercury activates phospholipase a(2) and induces formation of arachidonic acid metabolites in vascular endothelial cells. Toxicol Mech Methods. 2007;17(9):541-557. doi: 10.1080/15376510701380505</mixed-citation></citation-alternatives></ref><ref id="cit25"><label>25</label><citation-alternatives><mixed-citation xml:lang="ru">Kougias P, Chai H, Lin PH, Lumsden AB, Yao Q, Chen C. Lysophosphatidylcholine and secretory phospholipase A2 in vascular disease: mediators of endothelial dysfunction and atherosclerosis. Med Sci Monit. 2006;12(1):RA5-RA16.</mixed-citation><mixed-citation xml:lang="en">Kougias P, Chai H, Lin PH, Lumsden AB, Yao Q, Chen C. Lysophosphatidylcholine and secretory phospholipase A2 in vascular disease: mediators of endothelial dysfunction and atherosclerosis. Med Sci Monit. 2006;12(1):RA5-RA16.</mixed-citation></citation-alternatives></ref><ref id="cit26"><label>26</label><citation-alternatives><mixed-citation xml:lang="ru">Weber C, Noels H. Atherosclerosis: current pathogenesis and therapeutic options. Nat Med. 2011;17(11):1410-1422. doi: 10.1038/nm.2538</mixed-citation><mixed-citation xml:lang="en">Weber C, Noels H. Atherosclerosis: current pathogenesis and therapeutic options. Nat Med. 2011;17(11):1410-1422. doi: 10.1038/nm.2538</mixed-citation></citation-alternatives></ref><ref id="cit27"><label>27</label><citation-alternatives><mixed-citation xml:lang="ru">Kang GS, Gillespie PA, Gunnison A, Moreira AL, Tchou-Wong KM, Chen LC. Long-term inhalation exposure to nickel nanoparticles exacerbated atherosclerosis in a susceptible mouse model. Environ Health Perspect. 2011;119(2):176-181. doi: 10.1289/ehp.1002508</mixed-citation><mixed-citation xml:lang="en">Kang GS, Gillespie PA, Gunnison A, Moreira AL, Tchou-Wong KM, Chen LC. Long-term inhalation exposure to nickel nanoparticles exacerbated atherosclerosis in a susceptible mouse model. Environ Health Perspect. 2011;119(2):176-181. doi: 10.1289/ehp.1002508</mixed-citation></citation-alternatives></ref><ref id="cit28"><label>28</label><citation-alternatives><mixed-citation xml:lang="ru">Akerele OA, Cheema SK. Fatty acyl composition of lysophosphatidylcholine is important in atherosclerosis. Med Hypotheses. 2015;85(6):754-760. doi: 10.1016/j.mehy.2015.10.013</mixed-citation><mixed-citation xml:lang="en">Akerele OA, Cheema SK. Fatty acyl composition of lysophosphatidylcholine is important in atherosclerosis. Med Hypotheses. 2015;85(6):754-760. doi: 10.1016/j.mehy.2015.10.013</mixed-citation></citation-alternatives></ref><ref id="cit29"><label>29</label><citation-alternatives><mixed-citation xml:lang="ru">Khatana C, Saini NK, Chakrabarti S, et al. Mechanistic insights into the oxidized low-density lipoprotein-induced atherosclerosis. Oxid Med Cell Longev. 2020;2020:5245308. doi: 10.1155/2020/5245308</mixed-citation><mixed-citation xml:lang="en">Khatana C, Saini NK, Chakrabarti S, et al. Mechanistic insights into the oxidized low-density lipoprotein-induced atherosclerosis. Oxid Med Cell Longev. 2020;2020:5245308. doi: 10.1155/2020/5245308</mixed-citation></citation-alternatives></ref><ref id="cit30"><label>30</label><citation-alternatives><mixed-citation xml:lang="ru">Ragino YuI, Chernjavski AM, Polonskaya YaV, et al. Oxidation and endothelial dysfunction biomarkers of atherosclerotic plaque instability. Studies of the vascular wall and blood. Bull Exp Biol Med. 2012;153(3):331-335. doi: 10.1007/s10517-012-1708-6</mixed-citation><mixed-citation xml:lang="en">Ragino YuI, Chernjavski AM, Polonskaya YaV, et al. Oxidation and endothelial dysfunction biomarkers of atherosclerotic plaque instability. Studies of the vascular wall and blood. Bull Exp Biol Med. 2012;153(3):331-335. doi: 10.1007/s10517-012-1708-6</mixed-citation></citation-alternatives></ref><ref id="cit31"><label>31</label><citation-alternatives><mixed-citation xml:lang="ru">Zhou J, Austin RC. Contributions of hyperhomocysteinemia to atherosclerosis: Causal relationship and potential mechanisms. Biofactors. 2009;35(2):120-129. doi: 10.1002/biof.17</mixed-citation><mixed-citation xml:lang="en">Zhou J, Austin RC. Contributions of hyperhomocysteinemia to atherosclerosis: Causal relationship and potential mechanisms. Biofactors. 2009;35(2):120-129. doi: 10.1002/biof.17</mixed-citation></citation-alternatives></ref><ref id="cit32"><label>32</label><citation-alternatives><mixed-citation xml:lang="ru">Refsum H, Smith AD, Ueland PM, et al. Facts and recommendations about total homocysteine determinations: an expert opinion. Clin Chem. 2004;50(1):3-32. doi: 10.1373/clinchem.2003.021634</mixed-citation><mixed-citation xml:lang="en">Refsum H, Smith AD, Ueland PM, et al. Facts and recommendations about total homocysteine determinations: an expert opinion. Clin Chem. 2004;50(1):3-32. doi: 10.1373/clinchem.2003.021634</mixed-citation></citation-alternatives></ref><ref id="cit33"><label>33</label><citation-alternatives><mixed-citation xml:lang="ru">Zha W, A J, Wang G, et al. Metabonomic characterization of early atherosclerosis in hamsters with induced cholesterol. Biomarkers. 2009;14(6):372-380. doi: 10.1080/13547500903026401</mixed-citation><mixed-citation xml:lang="en">Zha W, A J, Wang G, et al. Metabonomic characterization of early atherosclerosis in hamsters with induced cholesterol. Biomarkers. 2009;14(6):372-380. doi: 10.1080/13547500903026401</mixed-citation></citation-alternatives></ref><ref id="cit34"><label>34</label><citation-alternatives><mixed-citation xml:lang="ru">Wang Z, Klipfell E, Bennett BJ, et al. Gut flora metabolism of phosphatidylcholine promotes cardiovascular disease. Nature. 2011;472(7341):57-63. doi: 10.1038/nature09922</mixed-citation><mixed-citation xml:lang="en">Wang Z, Klipfell E, Bennett BJ, et al. Gut flora metabolism of phosphatidylcholine promotes cardiovascular disease. Nature. 2011;472(7341):57-63. doi: 10.1038/nature09922</mixed-citation></citation-alternatives></ref><ref id="cit35"><label>35</label><citation-alternatives><mixed-citation xml:lang="ru">Jové M, Ayala V, Ramírez-Núñez O, et al. Lipidomic and metabolomic analyses reveal potential plasma biomarkers of early atheromatous plaque formation in hamsters. Cardiovasc Res. 2013;97(4):642-652. doi: 10.1093/cvr/cvs368</mixed-citation><mixed-citation xml:lang="en">Jové M, Ayala V, Ramírez-Núñez O, et al. Lipidomic and metabolomic analyses reveal potential plasma biomarkers of early atheromatous plaque formation in hamsters. Cardiovasc Res. 2013;97(4):642-652. doi: 10.1093/cvr/cvs368</mixed-citation></citation-alternatives></ref><ref id="cit36"><label>36</label><citation-alternatives><mixed-citation xml:lang="ru">Teul J, Rupérez FJ, Garcia A, et al. Improving metabolite knowledge in stable atherosclerosis patients by association and correlation of GC-MS and 1H NMR fingerprints. J Proteome Res. 2009;8(12):5580-5589. doi: 10.1021/pr900668v</mixed-citation><mixed-citation xml:lang="en">Teul J, Rupérez FJ, Garcia A, et al. Improving metabolite knowledge in stable atherosclerosis patients by association and correlation of GC-MS and 1H NMR fingerprints. J Proteome Res. 2009;8(12):5580-5589. doi: 10.1021/pr900668v</mixed-citation></citation-alternatives></ref><ref id="cit37"><label>37</label><citation-alternatives><mixed-citation xml:lang="ru">Cason CA, Dolan KT, Sharma G, et al. Plasma microbiome-modulated indole- and phenyl-derived metabolites associate with advanced atherosclerosis and postoperative outcomes. J Vasc Surg. 2018;68(5):1552-1562.e7. doi: 10.1016/j.jvs.2017.09.029</mixed-citation><mixed-citation xml:lang="en">Cason CA, Dolan KT, Sharma G, et al. Plasma microbiome-modulated indole- and phenyl-derived metabolites associate with advanced atherosclerosis and postoperative outcomes. J Vasc Surg. 2018;68(5):1552-1562.e7. doi: 10.1016/j.jvs.2017.09.029</mixed-citation></citation-alternatives></ref><ref id="cit38"><label>38</label><citation-alternatives><mixed-citation xml:lang="ru">Wang Q, Liu D, Song P, Zou MH. Tryptophan-kynurenine pathway is dysregulated in inflammation, and immune activation. Front Biosci (Landmark Ed). 2015;20(7):1116-1143. doi: 10.2741/4363</mixed-citation><mixed-citation xml:lang="en">Wang Q, Liu D, Song P, Zou MH. Tryptophan-kynurenine pathway is dysregulated in inflammation, and immune activation. Front Biosci (Landmark Ed). 2015;20(7):1116-1143. doi: 10.2741/4363</mixed-citation></citation-alternatives></ref><ref id="cit39"><label>39</label><citation-alternatives><mixed-citation xml:lang="ru">Niinisalo P, Oksala N, Levula M, et al. Activation of indoleamine 2,3-dioxygenase-induced tryptophan degradation in advanced atherosclerotic plaques: Tampere vascular study. Ann Med. 2010;42(1):55-63. doi: 10.3109/07853890903321559</mixed-citation><mixed-citation xml:lang="en">Niinisalo P, Oksala N, Levula M, et al. Activation of indoleamine 2,3-dioxygenase-induced tryptophan degradation in advanced atherosclerotic plaques: Tampere vascular study. Ann Med. 2010;42(1):55-63. doi: 10.3109/07853890903321559</mixed-citation></citation-alternatives></ref><ref id="cit40"><label>40</label><citation-alternatives><mixed-citation xml:lang="ru">Polyzos KA, Ketelhuth DF. The role of the kynurenine pathway of tryptophan metabolism in cardiovascular disease. An emerging field. Hamostaseologie. 2015;35(2):128-136. doi: 10.5482/HAMO-14-10-0052</mixed-citation><mixed-citation xml:lang="en">Polyzos KA, Ketelhuth DF. The role of the kynurenine pathway of tryptophan metabolism in cardiovascular disease. An emerging field. Hamostaseologie. 2015;35(2):128-136. doi: 10.5482/HAMO-14-10-0052</mixed-citation></citation-alternatives></ref><ref id="cit41"><label>41</label><citation-alternatives><mixed-citation xml:lang="ru">Song P, Ramprasath T, Wang H, Zou MH. Abnormal kynurenine pathway of tryptophan catabolism in cardiovascular diseases. Cell Mol Life Sci. 2017;74(16):2899-2916. doi: 10.1007/s00018-017-2504-2</mixed-citation><mixed-citation xml:lang="en">Song P, Ramprasath T, Wang H, Zou MH. Abnormal kynurenine pathway of tryptophan catabolism in cardiovascular diseases. Cell Mol Life Sci. 2017;74(16):2899-2916. doi: 10.1007/s00018-017-2504-2</mixed-citation></citation-alternatives></ref><ref id="cit42"><label>42</label><citation-alternatives><mixed-citation xml:lang="ru">Strehl C, Fangradt M, Fearon U, Gaber T, Buttgereit F, Veale DJ. Hypoxia: how does the monocyte– macrophage system respond to changes in oxygen availability? J Leukoc Biol. 2014;95(2):233-241. doi: 10.1189/jlb.1212627</mixed-citation><mixed-citation xml:lang="en">Strehl C, Fangradt M, Fearon U, Gaber T, Buttgereit F, Veale DJ. Hypoxia: how does the monocyte– macrophage system respond to changes in oxygen availability? J Leukoc Biol. 2014;95(2):233-241. doi: 10.1189/jlb.1212627</mixed-citation></citation-alternatives></ref><ref id="cit43"><label>43</label><citation-alternatives><mixed-citation xml:lang="ru">Будихина А.С., Пащенков М.В. Роль гликолиза в иммунном ответе // Иммунология. 2021. Т. 42. № 1. С. 5–20. doi: 10.33029/0206-4952-2021-42-1-5-20</mixed-citation><mixed-citation xml:lang="en">Budikhina AS, Pashenkov MV. The role of glycolysis in immune response. Immunologiya. 2021;42(1):5-20. (In Russ.) doi: 10.33029/0206-4952-2021-42-1-5-20</mixed-citation></citation-alternatives></ref><ref id="cit44"><label>44</label><citation-alternatives><mixed-citation xml:lang="ru">Коткина Т.И., Титов В.Н., Пархимович Р.М. Иные представления о β-окислении жирных кислот в пероксисомах, митохондриях и кетоновые тела. Диабетическая, ацидотическая кома как острый дефицит ацетил-КоА и АТФ // Клиническая лабораторная диагностика. 2014. Т. 59. № 3. С. 14–23.</mixed-citation><mixed-citation xml:lang="en">Kotkina TA, Titov VN, Parkhimovitch RM. The different notions about β-oxidation of fatty acids in peroxisomes, peroxisomes and ketonic bodies. The diabetic, acidotic coma as an acute deficiency of acetyl-KoA and ATPA. Klinicheskaya Laboratornaya Diagnostika. 2014;59(3):14-23. (In Russ.)</mixed-citation></citation-alternatives></ref><ref id="cit45"><label>45</label><citation-alternatives><mixed-citation xml:lang="ru">Shah SH, Sun JL, Stevens RD, et al. Baseline metabolomic profiles predict cardiovascular events in patients at risk for coronary artery disease. Am Heart J. 2012;163(5):844-850.e1. doi: 10.1016/j.ahj.2012.02.005</mixed-citation><mixed-citation xml:lang="en">Shah SH, Sun JL, Stevens RD, et al. Baseline metabolomic profiles predict cardiovascular events in patients at risk for coronary artery disease. Am Heart J. 2012;163(5):844-850.e1. doi: 10.1016/j.ahj.2012.02.005</mixed-citation></citation-alternatives></ref><ref id="cit46"><label>46</label><citation-alternatives><mixed-citation xml:lang="ru">Rutkowsky JM, Knotts TA, Ono-Moore KD, et al. Acylcarnitines activate proinflammatory signaling pathways. Am J Physiol Endocrinol Metab. 2014;306(12):E1378-E1387. doi: 10.1152/ajpendo.00656.2013</mixed-citation><mixed-citation xml:lang="en">Rutkowsky JM, Knotts TA, Ono-Moore KD, et al. Acylcarnitines activate proinflammatory signaling pathways. Am J Physiol Endocrinol Metab. 2014;306(12):E1378-E1387. doi: 10.1152/ajpendo.00656.2013</mixed-citation></citation-alternatives></ref><ref id="cit47"><label>47</label><citation-alternatives><mixed-citation xml:lang="ru">Gao X, Ke C, Liu H, et al. Large-scale metabolomic analysis reveals potential biomarkers for early stage coronary atherosclerosis. Sci Rep. 2017;7(1):11817. doi: 10.1038/s41598-017-12254-1</mixed-citation><mixed-citation xml:lang="en">Gao X, Ke C, Liu H, et al. Large-scale metabolomic analysis reveals potential biomarkers for early stage coronary atherosclerosis. Sci Rep. 2017;7(1):11817. doi: 10.1038/s41598-017-12254-1</mixed-citation></citation-alternatives></ref><ref id="cit48"><label>48</label><citation-alternatives><mixed-citation xml:lang="ru">Chen X, Liu L, Palacios G, et al. Plasma metabolomics reveals biomarkers of the atherosclerosis. J Sep Sci. 2010;33(17-18):2776-2783. doi: 10.1002/jssc.201000395</mixed-citation><mixed-citation xml:lang="en">Chen X, Liu L, Palacios G, et al. Plasma metabolomics reveals biomarkers of the atherosclerosis. J Sep Sci. 2010;33(17-18):2776-2783. doi: 10.1002/jssc.201000395</mixed-citation></citation-alternatives></ref><ref id="cit49"><label>49</label><citation-alternatives><mixed-citation xml:lang="ru">Blair HC, Sepulveda J, Papachristou DJ. Nature and nurture in atherosclerosis: The roles of acylcarnitine and cell membrane–fatty acid intermediates. Vascul Pharmacol. 2016;78:17-23. doi: 10.1016/j.vph.2015.06.012</mixed-citation><mixed-citation xml:lang="en">Blair HC, Sepulveda J, Papachristou DJ. Nature and nurture in atherosclerosis: The roles of acylcarnitine and cell membrane–fatty acid intermediates. Vascul Pharmacol. 2016;78:17-23. doi: 10.1016/j.vph.2015.06.012</mixed-citation></citation-alternatives></ref><ref id="cit50"><label>50</label><citation-alternatives><mixed-citation xml:lang="ru">Ghosh A, Gao L, Thakur A, Siu PM, Lai CWK. Role of free fatty acids in endothelial dysfunction. J Biomed Sci. 2017;24(1):50. doi: 10.1186/s12929-017-0357-5</mixed-citation><mixed-citation xml:lang="en">Ghosh A, Gao L, Thakur A, Siu PM, Lai CWK. Role of free fatty acids in endothelial dysfunction. J Biomed Sci. 2017;24(1):50. doi: 10.1186/s12929-017-0357-5</mixed-citation></citation-alternatives></ref><ref id="cit51"><label>51</label><citation-alternatives><mixed-citation xml:lang="ru">Wang L, Chen Y, Li X, Zhang Y, Gulbins E, Zhang Y. Enhancement of endothelial permeability by free fatty acid through lysosomal cathepsin B-mediated Nlrp3 inflammasome activation. Oncotarget. 2016;7(45):73229-73241. doi: 10.18632/oncotarget.12302</mixed-citation><mixed-citation xml:lang="en">Wang L, Chen Y, Li X, Zhang Y, Gulbins E, Zhang Y. Enhancement of endothelial permeability by free fatty acid through lysosomal cathepsin B-mediated Nlrp3 inflammasome activation. Oncotarget. 2016;7(45):73229-73241. doi: 10.18632/oncotarget.12302</mixed-citation></citation-alternatives></ref><ref id="cit52"><label>52</label><citation-alternatives><mixed-citation xml:lang="ru">Bismuth J, Lin P, Yao Q, Chen C. Ceramide: a common pathway for atherosclerosis? Atherosclerosis. 2008;196(2):497-504. doi: 10.1016/j.atherosclerosis.2007.09.018</mixed-citation><mixed-citation xml:lang="en">Bismuth J, Lin P, Yao Q, Chen C. Ceramide: a common pathway for atherosclerosis? Atherosclerosis. 2008;196(2):497-504. doi: 10.1016/j.atherosclerosis.2007.09.018</mixed-citation></citation-alternatives></ref><ref id="cit53"><label>53</label><citation-alternatives><mixed-citation xml:lang="ru">Vorkas PA, Shalhoub J, Isaac G, et al. Metabolic phenotyping of atherosclerotic plaques reveals latent associations between free cholesterol and ceramide metabolism in atherogenesis. J Proteome Res. 2015;14(3):1389-1399. doi: 10.1021/pr5009898</mixed-citation><mixed-citation xml:lang="en">Vorkas PA, Shalhoub J, Isaac G, et al. Metabolic phenotyping of atherosclerotic plaques reveals latent associations between free cholesterol and ceramide metabolism in atherogenesis. J Proteome Res. 2015;14(3):1389-1399. doi: 10.1021/pr5009898</mixed-citation></citation-alternatives></ref><ref id="cit54"><label>54</label><citation-alternatives><mixed-citation xml:lang="ru">Kinnunen PK, Holopainen JM. Sphingomyelinase activity of LDL: a link between atherosclerosis, ceramide, and apoptosis? Trends Cardiovasc Med. 2002;12(1):37-42. doi: 10.1016/s1050-1738(01)00143-8</mixed-citation><mixed-citation xml:lang="en">Kinnunen PK, Holopainen JM. Sphingomyelinase activity of LDL: a link between atherosclerosis, ceramide, and apoptosis? Trends Cardiovasc Med. 2002;12(1):37-42. doi: 10.1016/s1050-1738(01)00143-8</mixed-citation></citation-alternatives></ref><ref id="cit55"><label>55</label><citation-alternatives><mixed-citation xml:lang="ru">Chaurasia B, Summers SA. Ceramides – lipotoxic inducers of metabolic disorders. Trends Endocrinol Metab. 2015;26(10):538-550. doi: 10.1016/j.tem.2015.07.006</mixed-citation><mixed-citation xml:lang="en">Chaurasia B, Summers SA. Ceramides – lipotoxic inducers of metabolic disorders. Trends Endocrinol Metab. 2015;26(10):538-550. doi: 10.1016/j.tem.2015.07.006</mixed-citation></citation-alternatives></ref><ref id="cit56"><label>56</label><citation-alternatives><mixed-citation xml:lang="ru">Viola M, Bartolini B, Vigetti D, et al. Oxidized low density lipoprotein (LDL) affects hyaluronan synthesis in human aortic smooth muscle cells. J Biol Chem. 2013;288(41):29595-29603. doi: 10.1074/jbc.M113.508341</mixed-citation><mixed-citation xml:lang="en">Viola M, Bartolini B, Vigetti D, et al. Oxidized low density lipoprotein (LDL) affects hyaluronan synthesis in human aortic smooth muscle cells. J Biol Chem. 2013;288(41):29595-29603. doi: 10.1074/jbc.M113.508341</mixed-citation></citation-alternatives></ref><ref id="cit57"><label>57</label><citation-alternatives><mixed-citation xml:lang="ru">Takahashi T, Shimohata T. Vascular dysfunction induced by mercury exposure. Int J Mol Sci. 2019;20(10):2435. doi: 10.3390/ijms20102435</mixed-citation><mixed-citation xml:lang="en">Takahashi T, Shimohata T. Vascular dysfunction induced by mercury exposure. Int J Mol Sci. 2019;20(10):2435. doi: 10.3390/ijms20102435</mixed-citation></citation-alternatives></ref><ref id="cit58"><label>58</label><citation-alternatives><mixed-citation xml:lang="ru">Ivanova EA, Bobryshev YV, Orekhov AN. Intimal pericytes as the second line of immune defence in atherosclerosis. World J Cardiol. 2015;7(10):583-593. doi: 10.4330/wjc.v7.i10.583</mixed-citation><mixed-citation xml:lang="en">Ivanova EA, Bobryshev YV, Orekhov AN. Intimal pericytes as the second line of immune defence in atherosclerosis. World J Cardiol. 2015;7(10):583-593. doi: 10.4330/wjc.v7.i10.583</mixed-citation></citation-alternatives></ref><ref id="cit59"><label>59</label><citation-alternatives><mixed-citation xml:lang="ru">Lee DH, Lim JS, Song K, Boo Y, Jacobs DR Jr. Graded associations of blood lead and urinary cadmium concentrations with oxidative-stress-related markers in the U.S. population: results from the third National Health and Nutrition Examination Survey. Environ Health Perspect. 2006;114(3):350-354. doi: 10.1289/ehp.8518</mixed-citation><mixed-citation xml:lang="en">Lee DH, Lim JS, Song K, Boo Y, Jacobs DR Jr. Graded associations of blood lead and urinary cadmium concentrations with oxidative-stress-related markers in the U.S. population: results from the third National Health and Nutrition Examination Survey. Environ Health Perspect. 2006;114(3):350-354. doi: 10.1289/ehp.8518</mixed-citation></citation-alternatives></ref><ref id="cit60"><label>60</label><citation-alternatives><mixed-citation xml:lang="ru">Poręba R, Gać P, Poręba M, Andrzejak R. Environmental and occupational exposure to lead as a potential risk factor for cardiovascular disease. Environ Toxicol Pharmacol. 2011;31(2):267-277. doi: 10.1016/j.etap.2010.12.002</mixed-citation><mixed-citation xml:lang="en">Poręba R, Gać P, Poręba M, Andrzejak R. Environmental and occupational exposure to lead as a potential risk factor for cardiovascular disease. Environ Toxicol Pharmacol. 2011;31(2):267-277. doi: 10.1016/j.etap.2010.12.002</mixed-citation></citation-alternatives></ref><ref id="cit61"><label>61</label><citation-alternatives><mixed-citation xml:lang="ru">Seimon T, Tabas I. Mechanisms and consequences of macrophage apoptosis in atherosclerosis. J Lipid Res. 2009;50 Suppl(Suppl):S382-S387. doi: 10.1194/jlr.R800032-JLR200</mixed-citation><mixed-citation xml:lang="en">Seimon T, Tabas I. Mechanisms and consequences of macrophage apoptosis in atherosclerosis. J Lipid Res. 2009;50 Suppl(Suppl):S382-S387. doi: 10.1194/jlr.R800032-JLR200</mixed-citation></citation-alternatives></ref><ref id="cit62"><label>62</label><citation-alternatives><mixed-citation xml:lang="ru">Tabas I. The role of endoplasmic reticulum stress in the progression of atherosclerosis. Circ Res. 2010;107(7):839-850. doi: 10.1161/CIRCRESAHA.110.224766</mixed-citation><mixed-citation xml:lang="en">Tabas I. The role of endoplasmic reticulum stress in the progression of atherosclerosis. Circ Res. 2010;107(7):839-850. doi: 10.1161/CIRCRESAHA.110.224766</mixed-citation></citation-alternatives></ref><ref id="cit63"><label>63</label><citation-alternatives><mixed-citation xml:lang="ru">Watson KE, Boström K, Ravindranath R, Lam T, Norton B, Demer LL. TGF-beta 1 and 25-hydroxycholesterol stimulate osteoblast-like vascular cells to calcify. J Clin Invest. 1994;93(5):2106-2113. doi: 10.1172/JCI117205</mixed-citation><mixed-citation xml:lang="en">Watson KE, Boström K, Ravindranath R, Lam T, Norton B, Demer LL. TGF-beta 1 and 25-hydroxycholesterol stimulate osteoblast-like vascular cells to calcify. J Clin Invest. 1994;93(5):2106-2113. doi: 10.1172/JCI117205</mixed-citation></citation-alternatives></ref><ref id="cit64"><label>64</label><citation-alternatives><mixed-citation xml:lang="ru">Талаева Т.В., Братусь В.В. Сосудистая кальцификация: реальность и гипотезы. Медицинская газета Здоровье Украины XXI век. 2014. № 1 (32). С. 56–60.</mixed-citation><mixed-citation xml:lang="en">Talaeva TV, Bratus VV. Vascular calcification: reality and hypotheses. Meditsinskaya Gazeta Zdorov'e Ukrainy XXI vek. 2014;(1(32)):56-60. (In Russ.)</mixed-citation></citation-alternatives></ref><ref id="cit65"><label>65</label><citation-alternatives><mixed-citation xml:lang="ru">Fong GH. Potential contributions of intimal and plaque hypoxia to atherosclerosis. Curr Atheroscler Rep. 2015;17(6):510. doi: 10.1007/s11883-015-0510-0</mixed-citation><mixed-citation xml:lang="en">Fong GH. Potential contributions of intimal and plaque hypoxia to atherosclerosis. Curr Atheroscler Rep. 2015;17(6):510. doi: 10.1007/s11883-015-0510-0</mixed-citation></citation-alternatives></ref><ref id="cit66"><label>66</label><citation-alternatives><mixed-citation xml:lang="ru">Rafieian-Kopaei M, Setorki M, Doudi M, Baradaran A, Nasri H. Atherosclerosis: process, indicators, risk factors and new hopes. Int J Prev Med. 2014;5(8):927-946.</mixed-citation><mixed-citation xml:lang="en">Rafieian-Kopaei M, Setorki M, Doudi M, Baradaran A, Nasri H. Atherosclerosis: process, indicators, risk factors and new hopes. Int J Prev Med. 2014;5(8):927-946.</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>
