Consilium MedicumConsilium MedicumConsilium MedicumConsilium Medicum2075-17532542-2170Consilium Medicum62627610.26442/20751753.2023.10.202433ArticlesСтатьиReview ArticleMolecular mechanisms of inflammation in the development of heart failure: A reviewМолекулярные механизмы воспаления при развитии сердечной недостаточностиhttps://orcid.org/0000-0001-7016-7541BuziashviliYuri I.БузиашвилиЮрий Иосифович
Russian Federation

D. Sci. (Med.), Prof., Acad. RAS

акад. РАН, д-р мед. наук, проф., зав. клинико-диагностическим отд-нием

editor@omnidoctor.ruhttps://orcid.org/0000-0002-5422-2069AsymbekovaElmira U.АсымбековаЭльмира Уметовна
Russian Federation

D. Sci. (Med.)

д-р мед. наук, вед. науч. сотр. клинико-диагностического отд-ния

editor@omnidoctor.ruhttps://orcid.org/0000-0003-1751-4924TugeevaElvina F.ТугееваЭльвина Фаатовна
Russian Federation

D. Sci. (Med.)

д-р мед. наук, ст. науч. сотр. клинико-диагностического отд-ния

editor@omnidoctor.ruhttps://orcid.org/0000-0002-9370-9419RakhimovAkmal Z.РахимовАкмал Закрияевич
Russian Federation

Cand. Sci. (Med.)

канд. мед. наук, науч. сотр. клинико-диагностического отд-ния

editor@omnidoctor.ruhttps://orcid.org/0000-0001-7900-6728ShakhnazaryanLusine S.ШахназарянЛусине Самвеловна
Russian Federation

Cand. Sci. (Med.)

канд. мед. наук, врач-кардиолог клинико-диагностического отд-ния

editor@omnidoctor.ruhttps://orcid.org/0000-0002-1675-4216AkildzhonovFirdavsdzhon R.АкилджоновФирдавсджон Рустамджонович
Russian Federation

Graduate Student

аспирант клинико-диагностического отд-ния

firdavs96_tths@mail.ruBakulev National Medical Research Center of Cardiovascular SurgeryФГБУ «Национальный медицинский исследовательский центр сердечно-сосудистой хирургии им. А.Н. Бакулева» Минздрава России151020232510Cardiovascular diseasesБолезни сердца и сосудов6796843001202430012024Copyright ©; 2023, Consilium MedicumCopyright ©; 2023, ООО "Консилиум Медикум"2023Consilium MedicumООО "Консилиум Медикум"https://creativecommons.org/licenses/by-nc-sa/4.0https://consilium.orscience.ru/2075-1753/article/view/626276

Cardiovascular diseases continue to be the main cause of hospital mortality and lead to great disability of the working population. Numerous clinical and experimental studies have shown that inflammation is the main factor causing the growth and progression of atherosclerosis. Despite significant progress in basic therapy aimed at both preventing the development of heart failure (HF) and treating it, the prognosis in patients after their first hospitalization remains extremely unfavorable. HF is the leading cause of morbidity and mortality worldwide. Various stimuli at different stages of HF pathophysiology trigger a cascade of proinflammatory reactions with the release of interleukins, the formation of reactive oxygen species, mitochondrial DNA damage and the induction of autophagy. Based on the presented results from experimental and clinical studies, it can be expected that a better understanding of the molecular aspects in the pathophysiology of HF will open opportunities for the development of new therapeutic monoclonal antibodies.

Сердечно-сосудистые заболевания продолжают оставаться основной причиной госпитальной летальности и приводят к большой инвалидности трудоспособного населения. Многочисленные клинические и экспериментальные исследования показали, что воспаление является основным фактором, вызывающим рост и прогрессирование атеросклероза. Несмотря на значительный прогресс в базисной терапии, направленной как на профилактику развития сердечной недостаточности (СН), так и на лечение, прогноз у пациентов после их первой госпитализации остается крайне неблагоприятным. СН является ведущей причиной заболеваемости и смертности во всем мире. Различные стимулы на разных стадиях патофизиологии СН запускают каскад провоспалительных реакций с высвобождением интерлейкинов, образование активных форм кислорода, повреждение митохондриальной ДНК и индукцию аутофагии. Основываясь на представленных результатах экспериментальных и клинических исследований, можно ожидать, что лучшее понимание молекулярных аспектов в патофизиологии СН откроет возможности для разработки новых терапевтических моноклональных антител.

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