{"title":"[Inflammaging: the role of senescent cells in the pathogenesis of osteoarthritis.]","authors":"V N Khabarov, E S Mironova","doi":"","DOIUrl":null,"url":null,"abstract":"<p><p>Modern biogerontology considers cellular aging (senescence) as one of the main causes of general aging of the body. Any cell in the body can become senescent due to damage caused by both internal and external factors. Such cells can appear at the earliest stages of development and persist for many years. Due to the emergence of new highly effective research methods, significant progress has been made in recent years in studying and understanding the molecular mechanisms leading to senescence, as well as the effect of senescence on surrounding healthy cells in vitro and in vivo. The results of scientific studies presented in this review convincingly indicate that modern concepts of the pathogenesis of osteoarthritis cannot be formed without taking into account the role of senescent cells and such a process as inflammaging - progressive chronic sluggish systemic inflammation. In recent years, osteoarthritis has come to be considered as a process combining trauma and inflammation, since the key role of cytokines and immune cells in its pathogenesis has been established. Inflammaging is associated with increased numbers of senescent cells in osteoarthritic cartilage that secrete the aging-associated SASP phenotype. The proinflammatory environment initiated by SASP factors promotes cartilage degeneration and subchondral bone remodeling, ultimately leading to loss of cartilage function, osteoarthritis development, and disease progression.</p>","PeriodicalId":35293,"journal":{"name":"Advances in gerontology = Uspekhi gerontologii / Rossiiskaia akademiia nauk, Gerontologicheskoe obshchestvo","volume":"37 6","pages":"777-786"},"PeriodicalIF":0.0000,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Advances in gerontology = Uspekhi gerontologii / Rossiiskaia akademiia nauk, Gerontologicheskoe obshchestvo","FirstCategoryId":"1085","ListUrlMain":"","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q4","JCRName":"Medicine","Score":null,"Total":0}
引用次数: 0
Abstract
Modern biogerontology considers cellular aging (senescence) as one of the main causes of general aging of the body. Any cell in the body can become senescent due to damage caused by both internal and external factors. Such cells can appear at the earliest stages of development and persist for many years. Due to the emergence of new highly effective research methods, significant progress has been made in recent years in studying and understanding the molecular mechanisms leading to senescence, as well as the effect of senescence on surrounding healthy cells in vitro and in vivo. The results of scientific studies presented in this review convincingly indicate that modern concepts of the pathogenesis of osteoarthritis cannot be formed without taking into account the role of senescent cells and such a process as inflammaging - progressive chronic sluggish systemic inflammation. In recent years, osteoarthritis has come to be considered as a process combining trauma and inflammation, since the key role of cytokines and immune cells in its pathogenesis has been established. Inflammaging is associated with increased numbers of senescent cells in osteoarthritic cartilage that secrete the aging-associated SASP phenotype. The proinflammatory environment initiated by SASP factors promotes cartilage degeneration and subchondral bone remodeling, ultimately leading to loss of cartilage function, osteoarthritis development, and disease progression.