Lin Zicong, Deng Zhiqin, Liu Jianquan, Lin Zhongshi, Chen Siyu, Deng Zhenhan, Li Wencui
Hand and Foot Surgery Department, The First Affiliated Hospital of Shenzhen University, Shenzhen Second People's Hospital, Shenzhen, Guangdong, 518035, People's Republic of China.
Shenzhen Institute for Drug Control (Shenzhen Testing Center of Medical Devices), Shenzhen, Guangdong, 518057, People's Republic of China.
J Inflamm Res. 2022 Feb 11;15:953-964. doi: 10.2147/JIR.S350432. eCollection 2022.
Articular cartilage allows the human body to buffer and absorb stress during normal exercise. It is mainly composed of cartilage cells and the extracellular matrix and is surrounded by the extracellular microenvironment formed by synovial fluid and various factors in it. Studies have shown that chondrocytes are the metabolic center of articular cartilage. Under physiological conditions, the extracellular matrix is in a dynamic balance of anabolism and catabolism, and various factors and physical and chemical conditions in the extracellular microenvironment are also in a steady state. This homeostasis depends on the normal function of proteins represented by various ion channels on chondrocytes. In mammalian chondrocyte species, ion channels are mainly divided into two categories: cation channels and anion channels. Anion channels such as chloride channels have become hot research topics in recent years. These channels play an extremely important role in various physiological processes. Recently, a growing body of evidence has shown that many pathological processes, abnormal concentration of mechanical stress and chloride channel dysfunction in articular cartilage lead to microenvironment disorders, matrix and bone metabolism imbalances, which cause partial aseptic inflammation. These pathological processes initiate extracellular matrix degradation, abnormal chondrocyte death, hyperplasia of inflammatory synovium and bony. Osteoarthritis (OA) is a common clinical disease in orthopedics. Its typical manifestations are joint inflammation and pain caused by articular cartilage degeneration, but its pathogenesis has not been fully elucidated. Focusing on the physiological functions and pathological changes of chloride channels and pathophysiology of aseptic inflammation furthers the understanding of OA pathogenesis and provides possible targets for subsequent medication development.
关节软骨使人体在正常运动过程中能够缓冲和吸收应力。它主要由软骨细胞和细胞外基质组成，并被滑液及其所含各种因子形成的细胞外微环境所包围。研究表明，软骨细胞是关节软骨的代谢中心。在生理条件下，细胞外基质处于合成代谢和分解代谢的动态平衡中，细胞外微环境中的各种因子以及物理化学条件也处于稳定状态。这种稳态依赖于软骨细胞上各种离子通道所代表的蛋白质的正常功能。在哺乳动物软骨细胞种类中，离子通道主要分为两类：阳离子通道和阴离子通道。近年来，诸如氯离子通道等阴离子通道已成为热门研究课题。这些通道在各种生理过程中发挥着极其重要的作用。最近，越来越多的证据表明，关节软骨中的许多病理过程、机械应力浓度异常以及氯离子通道功能障碍会导致微环境紊乱、基质和骨代谢失衡，进而引发局部无菌性炎症。这些病理过程会引发细胞外基质降解、软骨细胞异常死亡、炎性滑膜增生和骨质增生。骨关节炎（OA）是骨科常见的临床疾病。其典型表现为由关节软骨退变引起的关节炎症和疼痛，但其发病机制尚未完全阐明。关注氯离子通道的生理功能、病理变化以及无菌性炎症的病理生理学，有助于深入了解OA的发病机制，并为后续药物研发提供可能的靶点。
