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软骨基质重塑的稳态与容积敏感离子通道的调节

The Homeostasis of Cartilage Matrix Remodeling and the Regulation of Volume-Sensitive Ion Channel.

作者信息

Deng Zhiqin, Chen Xiaoqiang, Lin Zicong, Alahdal Murad, Wang Daping, Liu Jianquan, Li Wencui

机构信息

Hand and Foot Surgery Department, Shenzhen Second People's Hospital/the First Hospital Affiliated to Shenzhen University, Shenzhen 518000, China.

出版信息

Aging Dis. 2022 Jun 1;13(3):787-800. doi: 10.14336/AD.2021.1122. eCollection 2022 Jun.

DOI:10.14336/AD.2021.1122
PMID:35656105
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9116913/
Abstract

Degenerative joint diseases of the hips and knees are common and are accompanied by severe pain and movement disorders. At the microscopic level, the main characteristics of osteoarthritis are the continuous destruction and degeneration of cartilage, increased cartilage extracellular matrix catabolism, decreased anabolism, increased synovial fluid, and decreased osmotic pressure. Cell volume stability is mainly regulated by ion channels, many of which are expressed in chondrocytes. These ion channels are closely related to pain regulation, volume regulation, the inflammatory response, cell proliferation, apoptosis, and cell differentiation. In this review, we focus on the important role of volume control-related ion channels in cartilage matrix remodeling and summarize current views. In addition, the potential mechanism of the volume-sensitive anion channel LRRC8A in the early occurrence of osteoarthritis is discussed.

摘要

髋部和膝部的退行性关节疾病很常见,且伴有严重疼痛和运动障碍。在微观层面,骨关节炎的主要特征是软骨持续破坏和退变、软骨细胞外基质分解代谢增加、合成代谢减少、滑液增多以及渗透压降低。细胞体积稳定性主要由离子通道调节,其中许多离子通道在软骨细胞中表达。这些离子通道与疼痛调节、体积调节、炎症反应、细胞增殖、凋亡及细胞分化密切相关。在本综述中,我们聚焦于与体积控制相关的离子通道在软骨基质重塑中的重要作用,并总结当前观点。此外,还讨论了容积敏感阴离子通道LRRC8A在骨关节炎早期发生中的潜在机制。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/00b2/9116913/a659b82b4e04/AD-13-3-787-g5.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/00b2/9116913/a659b82b4e04/AD-13-3-787-g5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/00b2/9116913/db207df885d9/AD-13-3-787-g1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/00b2/9116913/20b51ac0f766/AD-13-3-787-g2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/00b2/9116913/c7feb586659a/AD-13-3-787-g3.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/00b2/9116913/a659b82b4e04/AD-13-3-787-g5.jpg

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