mimmunМедицинская иммунологияMedical Immunology (Russia)1563-06252313-741XSPb RAACI10.15789/1563-0625-2019-2-201-208mimmun-1520Research ArticleОБЗОРЫREVIEWSРОЛЬ БЕЛКА ТЕПЛОВОГО ШОКА 70 В ПАТОГЕНЕЗЕ СЕРДЕЧНО-СОСУДИСТОЙ ПАТОЛОГИИTHE ROLE OF THE HEAT SHOCK PROTEIN 70 IN THE PATHOGENESIS OF CARDIOVASCULAR PATHOLOGYПонасенкоО. А.PonasenkoO. A.

студент-дипломник кафедры иммунологии МБФ

142115, г. Подольск, ул. Филиппова, 4а/46. Тел.: 8 (925) 275-65-86 

graduate student

ponasenko.oa@gmail.comГанковскаяЛ. В.GankovskayaL. V.

д.м.н., профессор, заведующая кафедрой иммунологии МБФ

PhD, MD (Medicine), Professor, Head, Department of Immunology

lvgan@yandex.ruСвитичО. А.SvitichO. A.

PhD, MD (Medicine), Corresponding Member, Russian Academy of Sciences, Head, Laboratory of Molecular Immunology

svitichoa@yandex.ruФГБОУ ВО «Российский национальный исследовательский медицинский университет имени Н.И. Пирогова»РоссияRussian National Research N.I. Pirogov Medical UniversityRussian FederationФГБОУ ВО «Российский национальный исследовательский медицинский университет имени Н.И. Пирогова»; ФГБНУ «Научно-исследовательский институт вакцин и сывороток имени И.И. Мечникова»Russian FederationRussian National Research N.I. Pirogov Medical UniversityRussian Federation201901032019212201208Copyright © Понасенко О.А., Ганковская Л.В., Свитич О.А., 20192019Понасенко О.А., Ганковская Л.В., Свитич О.А.Ponasenko O.A., Gankovskaya L.V., Svitich O.A.Данная работа распространяется под лицензией Creative Commons Attribution 4.0.This work is licensed under a Creative Commons Attribution 4.0 License.https://www.mimmun.ru/mimmun/article/view/2019-21-2-1

Проблема изучения сердечно-сосудистых заболеваний (ССЗ) на протяжении долгого времени остается чрезвычайно важной, и поэтому существует множество работ, в которых предлагаются новые способы диагностики и терапии данной группы заболеваний. Большие возможности дает изучение молекулярных взаимодействий для более точного понимания патогенеза сердечно-сосудистой патологии. Множество исследований в последнее время посвящено поиску маркеров риска развития ССЗ с целью более точной и ранней диагностики. В данной работе проведен анализ последних литературных данных, посвященных роли белка теплового шока 70 (HSP70) в сердечно-сосудистой патологии. Рассматривается его участие в таких процессах, как артериальная гипертензия, ишемическая болезнь сердца, атеросклероз. В атерогенезе большую роль играют сывороточные белки теплового шока 70. Доказано, что у пациентов с большой концентрацией циркулирующих в крови молекул белков теплового шока наблюдались увеличенные значения толщины комплекса интима-медиа сонных артерий. Отмечена важная роль антител к циркулирующим HSP70. Найдена ассоциация высоких уровней данных антител с атеросклерозом у пациентов с артериальной гипертензией в анамнезе, с инфарктом миокарда. Низкие уровни анти-HSP70-антител наблюдаются у пациентов с острым коронарным синдромом. Это доказывает сложность механизма и двоякую роль антител против сывороточных белков теплового шока 70. Таким образом, антитела против белков теплового шока 70 могут оцениваться как протективный маркер, так же как и предикторный, что требует дальнейшего изучения вопроса, а сами молекулы HSP70 могут каким-либо образом участвовать в развитии сердечно-сосудистых патологий. Большое внимание уделено роли воспалительного процесса и механизмам врожденного иммунитета при ССЗ. Так как в настоящее время считается, что эндогенные сигналы опасности (Danger-associated molecular patterns – DAMPs) вовлечены в патогенез этих патологий в контексте модели «опасности/повреждения». Согласно этой модели, пусковым фактором является стрессовое воздействие, ведущее к высвобождению DAMPs и их связыванию с рецепторами врожденного иммунитета – Toll-like receptors (TLRs). Активация TLRs запускает в клетке сигнальный каскад, ведущий к синтезу провоспалительных цитокинов. Это способствует развитию воспаления, которое может провоцировать появление новых патологических процессов в организме и ухудшать течение уже имеющихся заболеваний. Выявление новых потенциальных маркеров и знание молекулярных механизмов патогенеза ССЗ могут сыграть важную роль при разработке нового индивидуального подхода к профилактике сердечно-сосудистых заболеваний у пациентов.

The problem of studying cardiovascular diseases (CVD) for a long time remains extremely important, and, therefore, there are many works that offer new ways to diagnose and treat this group of diseases. Great opportunities are provided by the study of molecular interactions for a more accurate understanding of the pathogenesis of cardiovascular pathology. Many studies have recently been devoted to finding potential markers of CVD risk with the aim of more accurate and early diagnosis. In this review we analyze the latest literature data dedicated to the role of heat shock protein 70 (HSP70) in cardiovascular pathology. HSP70 take part in such processes as arterial hypertension, coronary heart disease, and atherosclerosis. In atherogenesis, serum heat shock proteins 70 play a major role. It has been proven that in patients with a high concentration of heat shock protein molecules circulating in the blood, increased values of the carotid intima-media complex were observed. The important role of antibodies to circulating HSP70 is noted. Found an association of high levels of these antibodies with atherosclerosis in patients with arterial hypertension in history, with myocardial infarction. Low levels of anti-HSP70 antibodies are observed in patients with acute coronary syndrome. This proves the complexity of the mechanism and the dual role of antibodies against serum heat shock proteins 70. Thus, antibodies against heat shock proteins 70 can be assessed as a protective marker, and as a predictor, which requires further study, and the HSP70 molecules themselves can somehow to participate in the development of cardiovascular pathologies. Much attention is paid to the role of the inflammatory process and the mechanisms of innate immunity in CVD. As it is currently believed that Danger-associated molecular patterns (DAMPs) are involved in the pathogenesis of these pathologies in the context of a “hazard/damage” model. According to this model, the triggering factor is stress, leading to the release of DAMPs and their binding to innate immunity receptors - Toll-like receptors (TLRs). Activation of TLRs triggers the signaling cascade in the cell leading to the synthesis of pro-inflammatory cytokines. This contributes to the development of inflammation, which can provoke the emergence of new pathological processes in the body and worsen the course of existing diseases. The identification of new potential markers and knowledge of the molecular mechanisms of the pathogenesis of CVD can play an important role in the development of a new individual approach to the prevention of cardiovascular diseases.

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The authors declare that there are no conflicts of interest present.