Zhang Chaofan, Lin Yunzhi, Yan Chun Hoi, Zhang Wenming
Department of Orthopaedic Surgery, The First Affiliated Hospital of Fujian Medical University, Fuzhou, China.
Department of Stomatology, The First Affiliated Hospital of Fujian Medical University, Fuzhou, China.
Front Bioeng Biotechnol. 2022 Apr 19;10:865370. doi: 10.3389/fbioe.2022.865370. eCollection 2022.
Osteoarthritis (OA) is a debilitating joint disease that affects millions of individuals. The pathogenesis of OA has not been fully elucidated. Obesity is a well-recognized risk factor for OA. Multiple studies have demonstrated adipokines play a key role in obesity-induced OA. Increasing evidence show that various adipokines may significantly affect the development or clinical course of OA by regulating the pro/anti-inflammatory and anabolic/catabolic balance, matrix remodeling, chondrocyte apoptosis and autophagy, and subchondral bone sclerosis. Several signaling pathways are involved but still have not been systematically investigated. In this article, we review the cellular and molecular mechanisms of adipokines in OA, and highlight the possible signaling pathways. The review suggested adipokines play important roles in obesity-induced OA, and exert downstream function the activation of various signaling pathways. In addition, some pharmaceuticals targeting these pathways have been applied into ongoing clinical trials and showed encouraging results. However, these signaling pathways are complex and converge into a common network with each other. In the future work, more research is warranted to further investigate how this network works. Moreover, more high quality randomised controlled trials are needed in order to investigate the therapeutic effects of pharmaceuticals against these pathways for the treatment of OA. This review may help researchers to better understand the pathogenesis of OA, so as to provide new insight for future clinical practices and translational research.
骨关节炎（OA）是一种使人衰弱的关节疾病，影响着数百万人。OA的发病机制尚未完全阐明。肥胖是OA公认的危险因素。多项研究表明，脂肪因子在肥胖诱导的OA中起关键作用。越来越多的证据表明，各种脂肪因子可能通过调节促炎/抗炎和合成代谢/分解代谢平衡、基质重塑、软骨细胞凋亡和自噬以及软骨下骨硬化，显著影响OA的发展或临床进程。涉及多种信号通路，但仍未得到系统研究。在本文中，我们综述了脂肪因子在OA中的细胞和分子机制，并强调了可能的信号通路。该综述表明，脂肪因子在肥胖诱导的OA中起重要作用，并通过激活各种信号通路发挥下游功能。此外，一些针对这些通路的药物已应用于正在进行的临床试验，并显示出令人鼓舞的结果。然而，这些信号通路很复杂，相互汇聚成一个共同的网络。在未来的工作中，需要更多的研究来进一步探究这个网络是如何运作的。此外，还需要更多高质量的随机对照试验，以研究针对这些通路的药物对OA的治疗效果。这篇综述可能有助于研究人员更好地理解OA的发病机制，从而为未来的临床实践和转化研究提供新的见解。
