[Inflammaging: the role of senescent cells in the pathogenesis of osteoarthritis.]

Q4 Medicine
V N Khabarov, E S Mironova
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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.

[炎症:衰老细胞在骨关节炎发病机制中的作用]
现代生物老年学认为细胞老化(衰老)是身体普遍衰老的主要原因之一。身体中的任何细胞都可能由于内部和外部因素造成的损伤而衰老。这样的细胞可以出现在发育的最初阶段,并持续多年。由于新的高效研究方法的出现,近年来在体外和体内对衰老的分子机制以及衰老对周围健康细胞的影响的研究和认识取得了重大进展。本综述中提出的科学研究结果令人信服地表明,如果不考虑衰老细胞的作用和炎症进行性慢性迟滞全身性炎症等过程,就不能形成骨关节炎发病机制的现代概念。近年来,由于细胞因子和免疫细胞在骨关节炎发病中的关键作用被确立,骨关节炎被认为是一个创伤和炎症相结合的过程。炎症与骨关节炎软骨中分泌与衰老相关的SASP表型的衰老细胞数量增加有关。SASP因子引发的促炎环境促进软骨退变和软骨下骨重塑,最终导致软骨功能丧失、骨关节炎的发生和疾病进展。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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来源期刊
CiteScore
0.50
自引率
0.00%
发文量
131
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