Regulation of chondrocyte apoptosis in osteoarthritis by endoplasmic reticulum stress

IF 3.3 3区生物学 Q3 CELL BIOLOGY

Cell Stress & Chaperones Pub Date : 2024-11-06 DOI:10.1016/j.cstres.2024.11.001

Renzhong Li , Kui Sun

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Abstract

Osteoarthritis (OA), a common degenerative joint disease, is characterized by the apoptosis of chondrocytes as a primary pathophysiological change, with endoplasmic reticulum stress (ERS) playing a crucial role. It has been demonstrated that an imbalance in endoplasmic reticulum (ER) homeostasis can lead to ERS, activating three cellular adaptive response pathways through the unfolded protein response to restore ER homeostasis. Mild ERS exerts a protective effect on cells, while prolonged ERS that disrupts the self-regulatory balance of the ER activates apoptotic signaling pathways, leading to chondrocyte apoptosis and hastening OA progression. Hence, controlling the ERS signaling pathway and its apoptotic factors has become a critical focus for preventing and treating OA. This review aims to elucidate the key mechanisms of ERS pathway-induced apoptosis, associated targets, and regulatory pathways, offering valuable insights to enhance the mechanistic understanding of OA. It also reviews the mechanisms studied for ERS-related drugs or compounds for the treatment of OA.

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内质网应激对骨关节炎中软骨细胞凋亡的调节作用

骨关节炎（OA）是一种常见的关节退行性疾病，以软骨细胞凋亡为主要病理生理变化，其中内质网应激（ERS）起着至关重要的作用。研究表明，内质网（ER）平衡失调可导致ERS，通过未折叠蛋白反应（UPR）激活三种细胞适应性反应途径，以恢复ER平衡。轻度的ERS对细胞有保护作用，而长时间的ERS会破坏内质网的自我调节平衡，激活细胞凋亡信号通路，导致软骨细胞凋亡，加速OA进展。因此，控制 ERS 信号通路及其凋亡因子已成为预防和治疗 OA 的关键重点。本综述旨在阐明ERS通路诱导凋亡的关键机制、相关靶点和调控途径，为加深对OA的机理认识提供有价值的见解。本综述还回顾了用于治疗 OA 的 ERS 相关药物或化合物的研究机制。

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

Cell Stress & Chaperones 生物-细胞生物学

CiteScore

7.60

自引率

2.60%

发文量

审稿时长

6-12 weeks

期刊介绍： Cell Stress and Chaperones is an integrative journal that bridges the gap between laboratory model systems and natural populations. The journal captures the eclectic spirit of the cellular stress response field in a single, concentrated source of current information. Major emphasis is placed on the effects of climate change on individual species in the natural environment and their capacity to adapt. This emphasis expands our focus on stress biology and medicine by linking climate change effects to research on cellular stress responses of animals, micro-organisms and plants.