<?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">cardiovascular</journal-id><journal-title-group><journal-title xml:lang="ru">Кардиоваскулярная терапия и профилактика</journal-title><trans-title-group xml:lang="en"><trans-title>Cardiovascular Therapy and Prevention</trans-title></trans-title-group></journal-title-group><issn pub-type="ppub">1728-8800</issn><issn pub-type="epub">2619-0125</issn><publisher><publisher-name>«SILICEA-POLIGRAF» LLC</publisher-name></publisher></journal-meta><article-meta><article-id pub-id-type="doi">10.15829/1728-8800-2026-4605</article-id><article-id custom-type="edn" pub-id-type="custom">FKUDVA</article-id><article-id custom-type="elpub" pub-id-type="custom">cardiovascular-4605</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>ХРОНИЧЕСКАЯ СЕРДЕЧНАЯ НЕДОСТАТОЧНОСТЬ</subject></subj-group><subj-group subj-group-type="section-heading" xml:lang="en"><subject>CHRONIC HEART FAILURE</subject></subj-group></article-categories><title-group><article-title>Анализ сывороточных концентраций каспаз-1, -8 и адипоцитокинов у больных с хронической сердечной недостаточностью с различной фракцией выброса</article-title><trans-title-group xml:lang="en"><trans-title>Analysis of serum concentrations of caspases-1, -8, and adipocytokines in patients with heart failure with different ejection fractions</trans-title></trans-title-group></title-group><contrib-group><contrib contrib-type="author" corresp="yes"><contrib-id contrib-id-type="orcid">https://orcid.org/0009-0004-4683-3355</contrib-id><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Рахмонова</surname><given-names>Ш. М.</given-names></name><name name-style="western" xml:lang="en"><surname>Rakhmanova</surname><given-names>Sh. M.</given-names></name></name-alternatives><bio xml:lang="ru"><p>аспирант отдела фундаментальных и прикладных аспектов ожирения</p><p>Москва</p></bio><bio xml:lang="en"><p>Moscow</p></bio><email xlink:type="simple">shahlo_rm@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/0000-0001-9305-6713</contrib-id><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Тимофеев</surname><given-names>Ю. С.</given-names></name><name name-style="western" xml:lang="en"><surname>Timofeev</surname><given-names>Yu. S.</given-names></name></name-alternatives><bio xml:lang="ru"><p>к.м.н., с.н.с., руководитель лаборатории изучения биохимических маркеров риска хронических неинфекционных заболеваний им. Н. В. Перовой отдела фундаментальных и прикладных аспектов ожирения</p><p>Москва</p><p> </p></bio><bio xml:lang="en"><p>Moscow</p></bio><email xlink:type="simple">YTimofeev@gnicpm.ru</email><xref ref-type="aff" rid="aff-1"/></contrib><contrib contrib-type="author" corresp="yes"><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Гострый</surname><given-names>А. В.</given-names></name><name name-style="western" xml:lang="en"><surname>Gostry</surname><given-names>A. V.</given-names></name></name-alternatives><bio xml:lang="ru"><p>м.н.с. отдела фундаментальных и прикладных аспектов ожирения</p><p>Москва</p></bio><bio xml:lang="en"><p>Moscow</p></bio><email xlink:type="simple">andrey.gostry@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/0000-0001-8665-9129</contrib-id><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Метельская</surname><given-names>В. А.</given-names></name><name name-style="western" xml:lang="en"><surname>Metelskaya</surname><given-names>V. A.</given-names></name></name-alternatives><bio xml:lang="ru"><p>профессор, г.н.с. лаборатории изучения биохимических маркеров риска хронических неинфекционных заболеваний им. Н. В. Перовой отдела фундаментальных и прикладных аспектов ожирения, профессор кафедры клинической лабораторной диагностики с курсом лабораторной иммунохимии</p><p>Москва</p><p> </p></bio><bio xml:lang="en"><p>Moscow</p></bio><email xlink:type="simple">vmetelskaya@gnicpm.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/0000-0002-5384-3795</contrib-id><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Джиоева</surname><given-names>О. Н.</given-names></name><name name-style="western" xml:lang="en"><surname>Dzhioeva</surname><given-names>O. N.</given-names></name></name-alternatives><bio xml:lang="ru"><p>д.м.н., доцент, в.н.с., руководитель лаборатории кардиовизуализации, вегетативной регуляции и сомнологии отдела фундаментальных и прикладных аспектов ожирения, профессор кафедры терапии и профилактической медицины</p><p>Москва</p></bio><bio xml:lang="en"><p>Moscow</p></bio><email xlink:type="simple">dzhioevaon@gmail.com</email><xref ref-type="aff" rid="aff-3"/></contrib><contrib contrib-type="author" corresp="yes"><contrib-id contrib-id-type="orcid">https://orcid.org/0000-0002-4453-8430</contrib-id><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Драпкина</surname><given-names>О. М.</given-names></name><name name-style="western" xml:lang="en"><surname>Drapkina</surname><given-names>O. M.</given-names></name></name-alternatives><bio xml:lang="ru"><p>д.м.н., профессор, академик РАН, директор</p><p>Москва</p></bio><bio xml:lang="en"><p>Moscow</p></bio><email xlink:type="simple">Drapkina@yandex.ru</email><xref ref-type="aff" rid="aff-1"/></contrib></contrib-group><aff-alternatives id="aff-1"><aff xml:lang="ru"><institution>ФГБУ "Национальный медицинский исследовательский центр терапии и профилактической медицины" Минздрава России</institution></aff><aff xml:lang="en"><institution>National Medical Research Center for Therapy and Preventive Medicine</institution></aff></aff-alternatives><aff-alternatives id="aff-2"><aff xml:lang="ru"><institution>ФГБУ "Национальный медицинский исследовательский центр терапии и профилактической медицины" Минздрава России; ФГБОУ ДПО "Российская медицинская академия непрерывного профессионального образования" Минздрава России</institution></aff><aff xml:lang="en"><institution>National Medical Research Center for Therapy and Preventive Medicine; Russian Medical Academy of Continuous Professional Education</institution></aff></aff-alternatives><aff-alternatives id="aff-3"><aff xml:lang="ru"><institution>ФГБУ "Национальный медицинский исследовательский центр терапии и профилактической медицины" Минздрава России; ФГБОУ ВО "Российский университет медицины" Минздрава России</institution></aff><aff xml:lang="en"><institution>National Medical Research Center for Therapy and Preventive Medicine; Russian University of Medicine</institution></aff></aff-alternatives><pub-date pub-type="collection"><year>2026</year></pub-date><pub-date pub-type="epub"><day>22</day><month>02</month><year>2026</year></pub-date><volume>25</volume><issue>1</issue><fpage>4605</fpage><lpage>4605</lpage><permissions><copyright-statement>Copyright &amp;#x00A9; Рахмонова Ш.М., Тимофеев Ю.С., Гострый А.В., Метельская В.А., Джиоева О.Н., Драпкина О.М., 2026</copyright-statement><copyright-year>2026</copyright-year><copyright-holder xml:lang="ru">Рахмонова Ш.М., Тимофеев Ю.С., Гострый А.В., Метельская В.А., Джиоева О.Н., Драпкина О.М.</copyright-holder><copyright-holder xml:lang="en">Rakhmanova S.M., Timofeev Y.S., Gostry A.V., Metelskaya V.A., Dzhioeva O.N., Drapkina O.M.</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://cardiovascular.elpub.ru/jour/article/view/4605">https://cardiovascular.elpub.ru/jour/article/view/4605</self-uri><abstract><sec><title>Цель</title><p>Цель. Провести сравнительный анализ комплекса биомаркеров программируемой клеточной гибели — каспаз-1, -8, адипоцитокинов — лептина, адипонектина и интерлейкина-6 (ИЛ-6) — у пациентов с хронической сердечной недостаточностью (ХСН) и у лиц без данного заболевания.</p></sec><sec><title>Материал и методы</title><p>Материал и методы. Обследованы 154 пациента в возрасте от 59 до 72 лет: 54 пациента с диагнозом ХСН в качестве основной группы и 100 пациентов без ХСН качестве группы контроля. Концентрации каспаз-1, -8, адипонектина, лептина и интерлейкина-6 определяли методом иммуноферментного анализа.</p></sec><sec><title>Результаты</title><p>Результаты. У пациентов с ХСН выявлены статистически значимо более высокие концентрации каспазы-1 и ИЛ-6, чем в группе контроля. С целью подтверждения потенциальной диагностической эффективности исследуемых биомаркеров был проведен ROC-анализ, который показал, что при сравнении группы пациентов с ХСН и группы контроля наиболее высокие площади под кривой были характерны для каспазы-1 и ИЛ-6. При анализе различий в зависимости от фракции выброса левого желудочка (ФВ ЛЖ) было выявлено, что медиана концентрации каспазы-8 при ХСН с низкой ФВ ЛЖ (ХСНнФВ) 422,2 [139,7-1246,2] пг/мл в 3 раза выше, чем в группе больных с ХСН с сохраненной ФВ ЛЖ — 126,8 [46,8- 293,5] пг/мл.</p></sec><sec><title>Заключение</title><p>Заключение. Выявлена связь сывороточных концентраций каспазы-1 и ИЛ-6 с наличием ХСН, при этом концентрация каспазы-8 ассоциировалась с ФВ ЛЖ и была статистически значимо более высокой в подгруппе с ХСНнФВ.</p></sec></abstract><trans-abstract xml:lang="en"><sec><title>Aim</title><p>Aim. To conduct a comparative analysis of a complex of programmed cell death biomarkers (caspases-1 and -8, adipocytokines — leptin, adiponectin, and interleukin-6 (IL-6)) in patients with heart failure (HF) and in individuals without this disease.</p></sec><sec><title>Material and methods</title><p>Material and methods. A total of 154 patients aged 59 to 72 years were examined: 54 patients with HF (study group) and 100 patients without HF (control group). Concentrations of caspases-1, -8, adiponectin, leptin, and interleukin-6 were determined using enzyme-linked immunosorbent assay.</p></sec><sec><title>Results</title><p>Results. Patients with HF had significantly higher concentrations of caspase-1 and IL-6 than those in the control group. To confirm the potential diagnostic efficacy of the studied biomarkers, a ROC analysis was performed. It showed that when comparing the group of patients with HF and the control group, the highest areas under the curve were characteristic of caspase-1 and IL-6. The median caspase-8 concentration in HF with reduced ejection fraction (HFrEF) 422,2 [139,7-1246,2] pg/ml is 3 times higher than in the group of patients with HF with preserved LVEF — 126,8 [46,8-293,5] pg/ml.</p></sec><sec><title>Conclusion</title><p>Conclusion. A relationship was found between serum concentrations of caspase-1 and IL-6 and HF, while the concentration of caspase-8 was associated with LVEF and was significantly higher in the subgroup with HFrEF.</p></sec></trans-abstract><kwd-group xml:lang="ru"><kwd>хроническая сердечная недостаточность</kwd><kwd>каспаза-1</kwd><kwd>каспаза-8</kwd><kwd>каспазы</kwd><kwd>адипокины</kwd><kwd>цитокины</kwd><kwd>биомаркеры</kwd><kwd>сыворотка крови</kwd></kwd-group><kwd-group xml:lang="en"><kwd>heart failure</kwd><kwd>caspase-1</kwd><kwd>caspase-8</kwd><kwd>caspases</kwd><kwd>adipokines</kwd><kwd>cytokines</kwd><kwd>biomarkers</kwd><kwd>serum</kwd></kwd-group><funding-group><funding-statement xml:lang="ru">Исследование проводилось в рамках государственного задания "Разработка информационно-аналитической системы для прогнозирования и улучшения исходов путем оптимизации подходов к ведению пациентов с декомпенсированной сердечной недостаточностью с сохраненной фракцией выброса с использованием мультимаркерной стратегии и методов искусственного интеллекта" (2025-2027гг, регистрационный номер И125011901994-4).</funding-statement><funding-statement xml:lang="en">The study was conducted as part of the state contract "Development of an information and analytical system for predicting and improving outcomes by optimizing approaches to managing patients with decompensated heart failure with preserved ejection fraction using a multimarker strategy and artificial intelligence methods" (2025-2027, registration number I125011901994-4).</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">Savarese G, Becher PM, Lund LH, et al. Global burden of heart failure: a comprehensive and updated review of epidemiology. Cardiovasc Res. 2023;118(17):3272-87. doi:10.1093/cvr/cvac013.</mixed-citation><mixed-citation xml:lang="en">Savarese G, Becher PM, Lund LH, et al. Global burden of heart failure: a comprehensive and updated review of epidemiology. Cardiovasc Res. 2023;118(17):3272-87. doi:10.1093/cvr/cvac013.</mixed-citation></citation-alternatives></ref><ref id="cit2"><label>2</label><citation-alternatives><mixed-citation xml:lang="ru">Поляков Д. С., Фомин И. В., Беленков Ю. Н. и др. Хроническая СН в Российской Федерации: что изменилось за 20 лет наблюдения? Результаты исследования ЭПОХА-ХСН. Кардиология. 2021;61(4):4-14. doi:10.18087/cardio.2021.4.n1628.</mixed-citation><mixed-citation xml:lang="en">Polyakov DS, Fomin IV, Belenkov YuN, et al. Chronic heart failure in the Russian Federation: what has changed over 20 years of follow up? Results of the EPOCH-CHF study. Kardiologiia. 2021;61(4):4-14. (In Russ.) doi:10.18087/cardio.2021.4.n1628.</mixed-citation></citation-alternatives></ref><ref id="cit3"><label>3</label><citation-alternatives><mixed-citation xml:lang="ru">Dye C, Cruz MD, Larsen T, et al. A review of the impact, pathophysiology, and management of atrial fibrillation in patients with heart failure with preserved ejection fraction. Am Heart J Plus. 2023;18:33:100309. doi:10.1016/j.ahjo.2023.100309.</mixed-citation><mixed-citation xml:lang="en">Dye C, Cruz MD, Larsen T, et al. A review of the impact, pathophysiology, and management of atrial fibrillation in patients with heart failure with preserved ejection fraction. Am Heart J Plus. 2023;18:33:100309. doi:10.1016/j.ahjo.2023.100309.</mixed-citation></citation-alternatives></ref><ref id="cit4"><label>4</label><citation-alternatives><mixed-citation xml:lang="ru">Amara M, Stoler O, Birati EY. The Role of Inflammation in the Pathophysiology of Heart Failure. Cells. 2025;14(14):1117. doi:10.3390/cells14141117.</mixed-citation><mixed-citation xml:lang="en">Amara M, Stoler O, Birati EY. The Role of Inflammation in the Pathophysiology of Heart Failure. Cells. 2025;14(14):1117. doi:10.3390/cells14141117.</mixed-citation></citation-alternatives></ref><ref id="cit5"><label>5</label><citation-alternatives><mixed-citation xml:lang="ru">Hanna A, Frangogiannis NG. Inflammatory Cytokines and Chemokines as Therapeutic Targets in Heart Failure. Cardiovasc Drugs Ther. 2020;34(6):849-63. doi:10.1007/s10557-020-07071-0.</mixed-citation><mixed-citation xml:lang="en">Hanna A, Frangogiannis NG. Inflammatory Cytokines and Chemokines as Therapeutic Targets in Heart Failure. Cardiovasc Drugs Ther. 2020;34(6):849-63. doi:10.1007/s10557-020-07071-0.</mixed-citation></citation-alternatives></ref><ref id="cit6"><label>6</label><citation-alternatives><mixed-citation xml:lang="ru">Chou CH, Hung CS, Liao CW, et al. IL-6 trans-signalling contributes to aldosterone-induced cardiac fibrosis. Cardiovasc Res. 2018;114:690-702. doi:10.1093/cvr/cvy013.</mixed-citation><mixed-citation xml:lang="en">Chou CH, Hung CS, Liao CW, et al. IL-6 trans-signalling contributes to aldosterone-induced cardiac fibrosis. Cardiovasc Res. 2018;114:690-702. doi:10.1093/cvr/cvy013.</mixed-citation></citation-alternatives></ref><ref id="cit7"><label>7</label><citation-alternatives><mixed-citation xml:lang="ru">Mir SA, Chatterjee A, Mitra AS, et al. Inhibition of signal transducer and activator of transcription 3 (STAT3) attenuates interleukin-6 (IL-6)-induced collagen synthesis and resultant hypertrophy in rat heart. J Biol Chem. 2012;287:2666-77. doi:10.1074/jbc.M111.246173.</mixed-citation><mixed-citation xml:lang="en">Mir SA, Chatterjee A, Mitra AS, et al. Inhibition of signal transducer and activator of transcription 3 (STAT3) attenuates interleukin- 6 (IL-6)-induced collagen synthesis and resultant hypertrophy in rat heart. J Biol Chem. 2012;287:2666-77. doi:10.1074/jbc.M111.246173.</mixed-citation></citation-alternatives></ref><ref id="cit8"><label>8</label><citation-alternatives><mixed-citation xml:lang="ru">Timper K, Denson JL, Steculorum SM, et al. IL-6 Improves Energy and Glucose Homeostasis in Obesity via Enhanced Central IL-6 trans-Signaling. Cell Rep. 2017;19(2):267-80. doi:10.1016/j.celrep.2017.03.043.</mixed-citation><mixed-citation xml:lang="en">Timper K, Denson JL, Steculorum SM, et al. IL-6 Improves Energy and Glucose Homeostasis in Obesity via Enhanced Central IL- 6 trans-Signaling. Cell Rep. 2017;19(2):267-80. doi:10.1016/j.celrep.2017.03.043.</mixed-citation></citation-alternatives></ref><ref id="cit9"><label>9</label><citation-alternatives><mixed-citation xml:lang="ru">Ozmen A, Nwabuobi C, Tang Z, et al. Leptin-Mediated Induction of IL-6 Expression in Hofbauer Cells Contributes to Preeclampsia Pathogenesis. Int J Mol Sci. 2023;25(1):135. doi:10.3390/ijms25010135.</mixed-citation><mixed-citation xml:lang="en">Ozmen A, Nwabuobi C, Tang Z, et al. Leptin-Mediated Induction of IL-6 Expression in Hofbauer Cells Contributes to Preeclampsia Pathogenesis. Int J Mol Sci. 2023;25(1):135. doi:10.3390/ijms25010135.</mixed-citation></citation-alternatives></ref><ref id="cit10"><label>10</label><citation-alternatives><mixed-citation xml:lang="ru">Sano E, Kazaana A, Tadakuma H, et al. Interleukin-6 sensitizes TNF-α and TRAIL/Apo2L dependent cell death through upregulation of death receptors in human cancer cells. Biochim Biophys Acta Mol Cell Res. 2021;1868(7):119037. doi:10.1016/j.bbamcr.2021.119037.</mixed-citation><mixed-citation xml:lang="en">Sano E, Kazaana A, Tadakuma H, et al. Interleukin-6 sensitizes TNF-α and TRAIL/Apo2L dependent cell death through upregulation of death receptors in human cancer cells. Biochim Biophys Acta Mol Cell Res. 2021;1868(7):119037. doi:10.1016/j.bbamcr.2021.119037.</mixed-citation></citation-alternatives></ref><ref id="cit11"><label>11</label><citation-alternatives><mixed-citation xml:lang="ru">Wu D, Deng D, Tang B. Programmed Cell Death in Heart Failure: Mechanisms, Impacts, and Therapeutic Prospects. Rev Cardiovasc Med. 2025;26(7):38407. doi:10.31083/RCM38407.</mixed-citation><mixed-citation xml:lang="en">Wu D, Deng D, Tang B. Programmed Cell Death in Heart Failure: Mechanisms, Impacts, and Therapeutic Prospects. Rev Cardiovasc Med. 2025;26(7):38407. doi:10.31083/RCM38407.</mixed-citation></citation-alternatives></ref><ref id="cit12"><label>12</label><citation-alternatives><mixed-citation xml:lang="ru">Zhou L, Sun J, Gu L, et al. Programmed Cell Death: Complex Regulatory Networks in Cardiovascular Disease. Front Cell Dev Biol. 2021; 26:9:794879. doi:10.3389/fcell.2021.794879.</mixed-citation><mixed-citation xml:lang="en">Zhou L, Sun J, Gu L, et al. Programmed Cell Death: Complex Regulatory Networks in Cardiovascular Disease. Front Cell Dev Biol. 2021; 26:9:794879. doi:10.3389/fcell.2021.794879.</mixed-citation></citation-alternatives></ref><ref id="cit13"><label>13</label><citation-alternatives><mixed-citation xml:lang="ru">Del Re DP, Amgalan D, Linkermann A, et al. Fundamental Mechanisms of Regulated Cell Death and Implications for Heart Disease. Physiol Rev. 2019;99(4):1765-817. doi:10.1152/physrev.00022.2018.</mixed-citation><mixed-citation xml:lang="en">Del Re DP, Amgalan D, Linkermann A, et al. Fundamental Mechanisms of Regulated Cell Death and Implications for Heart Disease. Physiol Rev. 2019;99(4):1765-817. doi:10.1152/physrev.00022.2018.</mixed-citation></citation-alternatives></ref><ref id="cit14"><label>14</label><citation-alternatives><mixed-citation xml:lang="ru">Buckley LF, Canada JM, Del Buono MG, et al. Low NT-proBNP levels in overweight and obese patients do not rule out a diagnosis of heart failure with preserved ejection fraction. ESC Heart fail. 2018;5(2):372-8. doi:10.1002/ehf2.12235.</mixed-citation><mixed-citation xml:lang="en">Buckley LF, Canada JM, Del Buono MG, et al. Low NT‐proBNP levels in overweight and obese patients do not rule out a diagnosis of heart failure with preserved ejection fraction. ESC Heart fail. 2018;5(2):372-8. doi:10.1002/ehf2.12235.</mixed-citation></citation-alternatives></ref><ref id="cit15"><label>15</label><citation-alternatives><mixed-citation xml:lang="ru">McDonagh T, Metra M. 2021 Рекомендации ESC по диагностике и лечению острой и хронической сердечной недостаточности. Российский кардиологический журнал. 2023;28(1):5168. doi:10.10.15829/1560-4071-2023-5168. EDN: SJMIKK.</mixed-citation><mixed-citation xml:lang="en">McDonagh TA, Metra M. 2021 ESC Guidelines for the diagnosis and treatment of acute and chronic heart failure. Russian Journal of Cardiology. 2023;28(1):5168. (In Russ.) doi:10.10.15829/1560-4071-2023-5168. EDN: SJMIKK.</mixed-citation></citation-alternatives></ref><ref id="cit16"><label>16</label><citation-alternatives><mixed-citation xml:lang="ru">Галявич А. С., Терещенко С. Н., Ускач Т. М. и др. Хроническая сердечная недостаточность. Клинические рекомендации 2024. Российский кардиологический журнал. 2024;29(11):6162. doi:10.15829/1560-4071-2024-6162.</mixed-citation><mixed-citation xml:lang="en">Galyavich AS, Tereshchenko SN, Uskach TM, et al. 2024 Clinical practice guidelines for Chronic heart failure. Russian Journal of Cardiology. 2024;29(11):6162. (In Russ.) doi:10.15829/1560-4071-2024-6162.</mixed-citation></citation-alternatives></ref><ref id="cit17"><label>17</label><citation-alternatives><mixed-citation xml:lang="ru">Смирнова М. П., Чижов П. А., Баранов А. А. и др. Маркеры воспаления интерлейкин-6, с-реактивный белок и гепсидин у больных с хронической сердечной недостаточностью и дефицитом железа. Вятский медицинский вестник. 2022;2(74):47-53. doi:10.24412/2220-7880-2022-274-47-53.</mixed-citation><mixed-citation xml:lang="en">Smirnova MP, Chizhov PA, Baranov AA, et al. Inflammation markers interleukin-6, c-reactive protein and hepcidin in chronic heart failure and iron deficiency patients. Medical newsletter of Vyatka. 2022;2(74):47-53. (In Russ.) doi:10.24412/2220-7880-2022-274-47-53.</mixed-citation></citation-alternatives></ref><ref id="cit18"><label>18</label><citation-alternatives><mixed-citation xml:lang="ru">Matsumoto M, Tsujino T, Lee-Kawabata M, et al. Serum interleukin-6 and C-reactive protein are markedly elevated in acute decompensated heart failure patients with left ventricular systolic dysfunction. Cytokine. 2010;49(3):264-8. doi:10.1016/j.cyto.2009.11.006.</mixed-citation><mixed-citation xml:lang="en">Matsumoto M, Tsujino T, Lee-Kawabata M, et al. Serum interleukin-6 and C-reactive protein are markedly elevated in acute decompensated heart failure patients with left ventricular systolic dysfunction. Cytokine. 2010;49(3):264-8. doi:10.1016/j.cyto.2009.11.006.</mixed-citation></citation-alternatives></ref><ref id="cit19"><label>19</label><citation-alternatives><mixed-citation xml:lang="ru">Анкудинов А. С., Калягин А. Н., Вихарева Е. Э. Ассоциации интерлейкина-6 и интерлейкина-10 с некоторыми показателями тяжести течения хронической сердечной недостаточности на фоне ревматоидного артрита. Забайкальский медицинский вестник. 2021;(2):10-7. doi:10.52485/19986173_2021_2_10.</mixed-citation><mixed-citation xml:lang="en">Ankudinov AS, Kalyagin AN, Vikhareva EE. Associations of interleukin- 6 and interleukin-10 with some indicators of the severity of chronic heart failure against the background of rheumatoid arthritis. Transbaikalian medical bulletin. 2021;(2):10-7. (In Russ.) doi:10.52485/19986173_2021_2_10.</mixed-citation></citation-alternatives></ref><ref id="cit20"><label>20</label><citation-alternatives><mixed-citation xml:lang="ru">Rauchhaus M, Doehner W, Francis DP, et al. Plasma cytokine parameters and mortality in patients with chronic heart failure. Circulation. 2000;102(25):3060-7. doi:10.1161/01.cir.102.25.3060.</mixed-citation><mixed-citation xml:lang="en">Rauchhaus M, Doehner W, Francis DP, et al. Plasma cytokine parameters and mortality in patients with chronic heart failure. Circulation. 2000;102(25):3060-7. doi:10.1161/01.cir.102.25.3060.</mixed-citation></citation-alternatives></ref><ref id="cit21"><label>21</label><citation-alternatives><mixed-citation xml:lang="ru">Loney L, Jackson CE, Adamson C, et al. Adverse Outcomes Associated With Interleukin-6 in Patients Recently Hospitalized for Heart Failure With Preserved Ejection Fraction. Circ Heart Fail. 2023;16(4):e010051. doi:10.1161/CIRCHEARTFAILURE.122.010051.</mixed-citation><mixed-citation xml:lang="en">Loney L, Jackson CE, Adamson C, et al. Adverse Outcomes Associated With Interleukin-6 in Patients Recently Hospitalized for Heart Failure With Preserved Ejection Fraction. Circ Heart Fail. 2023;16(4):e010051. doi:10.1161/CIRCHEARTFAILURE. 122.010051.</mixed-citation></citation-alternatives></ref><ref id="cit22"><label>22</label><citation-alternatives><mixed-citation xml:lang="ru">Hamzic-Mehmedbasic A. Inflammatory cytokines as risk factors for mortality after acute cardiac events. Med Arch. 2016; 70(4):252-5. doi:10.5455/medarh.2016.70.252-255.</mixed-citation><mixed-citation xml:lang="en">Hamzic-Mehmedbasic A. Inflammatory cytokines as risk factors for mortality after acute cardiac events. Med Arch. 2016; 70(4):252-5. doi:10.5455/medarh.2016.70.252-255.</mixed-citation></citation-alternatives></ref><ref id="cit23"><label>23</label><citation-alternatives><mixed-citation xml:lang="ru">Deng Y, Xie M, Li Q, et al. Targeting mitochondria-inflammation circuit by β-hydroxybutyrate mitigates HFpEF. Circ Res. 2021; 128(2):232-45. doi:10.1161/CIRCRESAHA.120.317933.</mixed-citation><mixed-citation xml:lang="en">Deng Y, Xie M, Li Q, et al. Targeting mitochondria-inflammation circuit by β-hydroxybutyrate mitigates HFpEF. Circ Res. 2021; 128(2):232-45. doi:10.1161/CIRCRESAHA.120.317933.</mixed-citation></citation-alternatives></ref><ref id="cit24"><label>24</label><citation-alternatives><mixed-citation xml:lang="ru">Zeng C, Duan F, Hu J, et al. NLRP3 inflammasome-mediated pyroptosis contributes to the pathogenesis of non-ischemic dilated cardiomyopathy. Redox Biol. 2020;34:101523. doi:10.1016/j.redox.2020.101523.</mixed-citation><mixed-citation xml:lang="en">Zeng C, Duan F, Hu J, et al. NLRP3 inflammasome-mediated pyroptosis contributes to the pathogenesis of non-ischemic dilated cardiomyopathy. Redox Biol. 2020;34:101523. doi:10.1016/j.redox.2020.101523.</mixed-citation></citation-alternatives></ref><ref id="cit25"><label>25</label><citation-alternatives><mixed-citation xml:lang="ru">Логаткина А. В., Бондарь С. С., Аржников В. В. Продукция цитокинов, растворимых форм костимуляторных молекул и окиси азота у пациентов с ишемической болезнью сердца на фоне низкоинтенсивной микроволновой терапии. Вестник новых медицинских технологий. 2016;10(1):82-92. doi:10.12737/18560.</mixed-citation><mixed-citation xml:lang="en">Logatkina AV, Bondar SS, Arjnikov VV. The conditions of production of cytokines, soluble of co-stimulatory molecules, intracellular signaling pathways and nitric oxide in patients with coronary heart disease on the background of low-intensity microwave therapy. Journal of New Medical Technologies. 2016;10(1):82-92. (In Russ.) doi:10.12737/18560.</mixed-citation></citation-alternatives></ref><ref id="cit26"><label>26</label><citation-alternatives><mixed-citation xml:lang="ru">Shi X, Xie WL, Kong WW, et al. Expression of the NLRP3 inflammasome in carotid atherosclerosis. J Stroke Cerebrovasc Dis. 2015;24(11):2455-66. doi:10.1016/j.jstrokecerebrovasdis.2015.03.024.</mixed-citation><mixed-citation xml:lang="en">Shi X, Xie WL, Kong WW, et al. Expression of the NLRP3 inflammasome in carotid atherosclerosis. J Stroke Cerebrovasc Dis. 2015;24(11):2455-66. doi:10.1016/j.jstrokecerebrovasdis.2015. 03.024.</mixed-citation></citation-alternatives></ref><ref id="cit27"><label>27</label><citation-alternatives><mixed-citation xml:lang="ru">Попов С. С., Пашков А. Н., Есауленко И. Э. и др. Антиапоптотическое действие мелатонина при неалкогольном стеатогепатите, развивающемся при сахарном диабете 2-го типа. Проблемы эндокринологии. 2017; 63(3):162-8. doi:10.14341/probl2017633162-168.</mixed-citation><mixed-citation xml:lang="en">Popov SS, Pashkov AN, Esaulenko IE, et al. Antiapoptotic effect of melatonin in nonalcoholic steatohepatitis developing in patients with type 2 diabetes mellitus. Problems of Endocrinology. 2017;63(3):162-8. (In Russ.) doi:10.14341/probl2017633162-168.</mixed-citation></citation-alternatives></ref><ref id="cit28"><label>28</label><citation-alternatives><mixed-citation xml:lang="ru">Zhang Y, Huang Y, Hu S, et al. Associations between plasma caspase-1 levels and cardiovascular disease, with the mediating role of metabolic syndrome. Atherosclerosis. 2025;401:119090. doi:10.1016/j.atherosclerosis.2024.119090.</mixed-citation><mixed-citation xml:lang="en">Zhang Y, Huang Y, Hu S, et al. Associations between plasma caspase-1 levels and cardiovascular disease, with the mediating role of metabolic syndrome. Atherosclerosis. 2025;401:119090. doi:10.1016/j.atherosclerosis.2024.119090.</mixed-citation></citation-alternatives></ref><ref id="cit29"><label>29</label><citation-alternatives><mixed-citation xml:lang="ru">Драпкина О. М., Шепель Р. Н., Деева Т. А. Изучение степени апоптоза у пациентов с метаболическим синдромом путем оценки уровня каспазы-8 в плазме крови. Неотложная кардиология и кардиоваскулярные риски. 2017;1(1):79-83.</mixed-citation><mixed-citation xml:lang="en">Drapkina OM, Shepel RN, Deeva TA. The Study of the Extent of Apoptosis in Patients With Metabolic Syndrome by Assessing the Level of Caspase-8 in Blood Plasma. Neotlozhnaya kardiologiya i kardioovaskulyarnye riski [Emergency cardiology and cardiovascular risks]. 2017;1(1):79-83. (In Russ.)</mixed-citation></citation-alternatives></ref><ref id="cit30"><label>30</label><citation-alternatives><mixed-citation xml:lang="ru">Горшунова Н. К., Шевченко Ю. Ф. Патогенетическое значение маркеров субклинического воспаления и апоптоза при эссенциальной артериальной гипертензии у женщин пожилого возраста. Регионарное кровообращение и микроциркуляция. 2020; 19(1):47-52. doi:10.24884/1682-6655-2020-19-1-47-52.</mixed-citation><mixed-citation xml:lang="en">Gorshunova NK, Shevchenko YuF. Pathogenetic significance of subclinical inflammatory and apoptotic markers in elderly women with essential arterial hypertension. Regional hemodynamics and microcirculation. 2020;19(1):47-52. (In Russ.) doi:10.24884/1682-6655-2020-19-1-47-52.</mixed-citation></citation-alternatives></ref><ref id="cit31"><label>31</label><citation-alternatives><mixed-citation xml:lang="ru">Olivetti G, Abbi R, Quaini F, et al. Apoptosis in the failing human heart. N Engl J Med. 1997;336(16):1131-41. doi:10.1056/NEJM199704173361603.</mixed-citation><mixed-citation xml:lang="en">Olivetti G, Abbi R, Quaini F, et al. Apoptosis in the failing human heart. N Engl J Med. 1997;336(16):1131-41. doi:10.1056/NEJM199704173361603.</mixed-citation></citation-alternatives></ref><ref id="cit32"><label>32</label><citation-alternatives><mixed-citation xml:lang="ru">Pang J, Vince JE. The role of caspase-8 in inflammatory signalling and pyroptotic cell death. Semin Immunol. 2023;70:101832. doi:10.1016/j.smim.2023.101832.</mixed-citation><mixed-citation xml:lang="en">Pang J, Vince JE. The role of caspase-8 in inflammatory signalling and pyroptotic cell death. Semin Immunol. 2023;70:101832. doi:10.1016/j.smim.2023.101832.</mixed-citation></citation-alternatives></ref><ref id="cit33"><label>33</label><citation-alternatives><mixed-citation xml:lang="ru">Petrilli V, Papin S, Dostert C, et al. Activation of the NALP3 inflammasome is triggered by low intracellular potassium concentration. Cell Death Differ. 2007;14(9):1583-9. doi:10.1038/sj.cdd.4402195.</mixed-citation><mixed-citation xml:lang="en">Petrilli V, Papin S, Dostert C, et al. Activation of the NALP3 inflammasome is triggered by low intracellular potassium concentration. Cell Death Differ. 2007;14(9):1583-9. doi:10.1038/sj.cdd.4402195.</mixed-citation></citation-alternatives></ref><ref id="cit34"><label>34</label><citation-alternatives><mixed-citation xml:lang="ru">Muñoz-Planillo R, Kuffa P, et al. K+-efflux is the common trigger of NLRP3 inflammasome activation by bacterial toxins and particulate matter. Immunity. 2013;27:38(6):1142-53. doi:10.1016/j.immuni.2013.05.016.</mixed-citation><mixed-citation xml:lang="en">Muñoz-Planillo R, Kuffa P, et al. K+-efflux is the common trigger of NLRP3 inflammasome activation by bacterial toxins and particulate matter. Immunity. 2013;27:38(6):1142-53. doi:10. 1016/j.immuni.2013.05.016.</mixed-citation></citation-alternatives></ref><ref id="cit35"><label>35</label><citation-alternatives><mixed-citation xml:lang="ru">Chen KW, Demarco B, Heilig R, et al. Extrinsic and intrinsic apoptosis activate pannexin-1 to drive NLRP 3 inflammasome assembly. EMBO J. 2019;38(10):e101638. doi:10.15252/embj.2019101638.</mixed-citation><mixed-citation xml:lang="en">Chen KW, Demarco B, Heilig R, et al. Extrinsic and intrinsic apoptosis activate pannexin‐1 to drive NLRP 3 inflammasome assembly. EMBO J. 2019;38(10):e101638. doi:10.15252/embj.2019101638.</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>
