russjcardiolРоссийский кардиологический журналRussian Journal of Cardiology1560-40712618-7620«SILICEA-POLIGRAF» LLC10.15829/1560-4071-2020-3933russjcardiol-3933Research ArticleПРОБЛЕМНАЯ СТАТЬЯБиомаркеры фиброза миокарда и их генетическое регулирование у пациентов с сердечной недостаточностьюBiomarkers of myocardial fibrosis and their genetic regulation in patients with heart failurehttps://orcid.org/0000-0002-4771-484XПечеринаТ. Б.PecherinaT. B.

Тамара Борзалиевна Печерина —кандидат медицинских наук, старший научный сотрудник лаборатории патологии кровообращения отдела клинической кардиологии НИИ КПССЗ, старший преподаватель, доцент

Кемерово

tb.pechorina@gmail.comhttps://orcid.org/0000-0001-8679-4857КутихинА. Г.KutikhinA. G.

Антон Геннадьевич Кутихин — к.м.н., зав. лабораторией фундаментальных аспектов атеросклероза отдела экспериментальной медицины

Кемерово

antonkutikhin@gmail.comФГБНУ Научно-исследовательский институт комплексных проблем сердечнососудистых заболеванийРоссияResearch Institute for Complex Issues of Cardiovascular DiseasesRussian Federation202014072020251039333933Copyright © Печерина Т.Б., Кутихин А.Г., 20202020Печерина Т.Б., Кутихин А.Г.Pecherina T.B., Kutikhin A.G.This work is licensed under a Creative Commons Attribution 4.0 License.https://russjcardiol.elpub.ru/jour/article/view/3933

В настоящее время развитие хронической сердечной недостаточности рассматривается с позиции патологического структурного ремоделирования миокарда и фиброза. Несмотря на существование в клинической практике молекулярно-генетических маркеров, лишь небольшое число из них используется для оценки процессов ремоделирования и прогнозирования потенциальных осложнений, ассоциированных с сердечной недостаточностью. Кроме того, до сих пор не определена связь между многими биомаркерами с инструментальным и гистологическим подтверждением фиброза миокарда.

Позиция изучения фиброза миокарда остается достаточно дискутабельной и противоречивой, что актуализирует дальнейшее изучение этого направления. Открытие патогенетических и диагностических маркеров, объективно отражающих развитие фиброза миокарда, могло бы способствовать разработке таргетной терапии для лечения данной патологии. Особый интерес представляет собой поиск возможных маркеров патогенеза, имеющих диагностическое и терапевтическое значение, поскольку это имеет непосредственную ценность для клинической практики.

Currently, the development of chronic heart failure (CHF) is considered from the perspective of pathological structural remodeling of myocardium and fibrosis. Despite the widespread use of molecular genetic markers in clinical practice, only a small number of them are used to evaluate remodeling processes, as well as to predict potential complications associated with heart failure (HF). In addition, the relationship between many biomarkers with instrumental and histological confirmation of myocardial fibrosis has not yet been determined. Myocardial fibrosis remains quite debatable and controversial subject, which actualizes the further study of this direction. The discovery of pathogenetic and diagnostic markers of myocardial fibrosis could contribute to the development of targeted therapy. Of particular interest is the search for possible pathogenetic markers, since this is relevant for clinical practice.

хроническая сердечная недостаточностьфиброз миокардабиомаркерыгенетическое регулирование.heart failuremyocardial fibrosisbiomarkersgenetic regulationИсследование выполнено при финансовой поддержке РФФИ и Кемеровской области в рамках научного проекта № 18-415420004 “Молекулярно-генетические маркеры фиброза при постинфарктном ремоделировании миокарда”.The study was financially supported by the Russian Foundation for Basic Research and the Kemerovo Region within the project № 18-415-420004 “Molecular genetic markers of fibrosis in postinfarct myocardial remodeling”.ReferencesGBD 2017 Causes of Death Collaborators. Global, regional, and national age-sex-specific mortality for 282 causes of death in 195 countries and territories, 1980-2017: a systematic analysis for the Global Burden of Disease Study 2017. Lancet. 2018;392(10159):1736-1788. doi: 10.1016/S0140-6736(18)32203-7.GBD 2017 Causes of Death Collaborators. 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The authors declare that there are no conflicts of interest present.