Cytokines and inflammationCytokines and inflammationЦитокины и воспаление1684-7849Eco-Vector69380510.17816/CI693805NOIESWReviewsНаучные обзорыReview ArticleThe role of pro- and anti-inflammatory cytokines in the pathogenesis of acute and chronic kidney injuryПро- и противовоспалительные цитокины в патогенезе острого и хронического повреждения почекhttps://orcid.org/0000-0001-9641-01591231-5948FisenkoVasily G.ФисенкоВасилий Геннадьевич
Russian Federation

Medical Complex

Медицинский комплекс

fishmendoc@mail.ruhttps://orcid.org/0000-0003-1085-36325018-1630ZdorVictoria V.ЗдорВиктория Владимировна
Russian Federation

MD, Dr. Sci. (Medicine)

д-р мед. наук

Victoria.zdor@mail.ruhttps://orcid.org/0000-0001-5846-851X3661-5026MarkelovaElena V.МаркеловаЕлена Владимировна
Russian Federation

MD, Dr. Sci. (Medicine), Professor

д-р мед. наук, профессор

markelova.ev@tgmu.ruPacific State Medical UniversityТихоокеанский государственный медицинский университетFar Eastern Federal UniversityДальневосточный федеральный университетDiabetes and Endocrine Diseases ClinicКлиника диабета и эндокринных заболеваний241120253011202522112191910202520112025Copyright ©; 2025, Eco-VectorCopyright ©; 2025, Эко-Вектор2025Eco-VectorЭко-Векторhttps://creativecommons.org/licenses/by-nc-nd/4.0/https://cijournal.ru/1684-7849/article/view/693805

Over the past decade, immunology research has focused on immunological markers and molecular predictors of chronic kidney disease progression, and the causes of acute kidney injury associated with atherosclerosis and diabetes mellitus. Understanding the precise immunological mechanisms of a disease is essential for modifying its progression, increasing patients’ active life expectancy, and eliminating the need for extracorporeal treatment procedures. Studies have shown common immune and inflammatory mechanisms in chronic kidney disease that are present in various human conditions. These mechanisms suggest that inflammation, apoptosis, and fibrosis replace renal parenchyma with connective tissue. Progressive inflammation leads to decreased number of functioning nephrons and causes the loss of normal renal parenchyma. This process forms the pathogenetic basis for chronic kidney disease, a potential complication of an underlying disease. Studies have shown that in atherosclerosis, diabetic nephropathy, and some other comorbidities, even a single event of acute kidney injury can lead to a chronic condition. This is because acute kidney injury can progress rapidly to chronic kidney disease, resulting in increased inflammation, apoptosis, and fibrosis. Understanding these mechanisms and their mediators provides new insights into immunotherapy for renal fibrosis and its impact on the progression of chronic kidney disease. This review focuses on research into the role of cytokines in the progression of renal parenchymal fibrosis, as well as new in vivo options for targeting this process.

В последнее 10-летие изучение иммунологических маркёров и молекулярных предикторов прогрессирования хронической болезни почек и уточнение причин возникновения острого повреждения почек при коморбидности с атеросклерозом и сахарным диабетом стало одной из весьма актуальных задач иммунологии. Установление точных иммунологических механизмов патологии представляет собой реальную возможность в дальнейшем влиять на течение заболевания и на увеличение продолжительности полноценной жизни пациентов без применения экстракорпоральных методов лечения. Научные исследования привели к доказательству наличия общих иммуновоспалительных механизмов хронической болезни почек при разной патологии человека, свидетельствуя о том, что через воспаление, апоптоз и фиброз происходит структурная замена паренхимы почки соединительной тканью. Прогрессирующее воспаление приводит к снижению количества функционирующих нефронов и потере нормальной паренхимы почек, что является основой патогенеза хронической болезни почек как осложнения основного заболевания. Было показано, что при атеросклерозе, диабетической нефропатии и ряде других состояний даже однократное развитие острого повреждения почек может иметь долгосрочные последствия, поскольку способно быстро прогрессировать до хронической болезни почек путём усиления воспаления, апоптоза и фиброза почечной ткани. Уточнение этих механизмов и регулирующих их медиаторов открывает новые перспективы в иммунотерапии почечного фиброза и воздействии на прогрессирование хронической болезни почек. Данный обзор посвящён научным исследованиям о роли цитокинов в прогрессировании фиброза почечной паренхимы и новым возможностям таргетного воздействия на данный патологический процесс in vivo.

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