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作 者:Zeyu Han Ketao Wang Shenglong Ding Mingzhu Zhang
出 处:《Bone Research》2024年第4期766-782,共17页骨研究(英文版)
基 金:supported by the Beijing Hospitals Authority’s Ascent Plan;the National Natural Science Foundation of China (82272473,82402805);the Talent Development Plan for High-level Public Health Technical Personnel Project (Subject leader-02-23);the Beijing Natural Science Foundation Haidian Original Innovation Joint Fund (L212010);the Priming Scientific Research Foundation for the Junior Researcher in Beijing Tongren Hospital (2023-YJJ-ZZL-016)。
摘 要:Osteoarthritis (OA) poses a significant challenge in orthopedics. Inflammatory pathways are regarded as central mechanisms in the onset and progression of OA. Growing evidence suggests that senescence acts as a mediator in inflammation-induced OA. Given the lack of effective treatments for OA, there is an urgent need for a clearer understanding of its pathogenesis. In this review, we systematically summarize the cross-talk between cellular senescence and inflammation in OA. We begin by focusing on the mechanisms and hallmarks of cellular senescence, summarizing evidence that supports the relationship between cellular senescence and inflammation. We then discuss the mechanisms of interaction between cellular senescence and inflammation, including senescence-associated secretory phenotypes (SASP) and the effects of pro- and anti-inflammatory interventions on cellular senescence. Additionally, we focus on various types of cellular senescence in OA, including senescence in cartilage, subchondral bone, synovium, infrapatellar fat pad, stem cells, and immune cells, elucidating their mechanisms and impacts on OA. Finally, we highlight the potential of therapies targeting senescent cells in OA as a strategy for promoting cartilage regeneration.
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