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骨骼系统中组织蛋白酶K非破骨细胞:功能、模型、特性及治疗意义

Cathepsin K Non-Osteoclast Cells in the Skeletal System: Function, Models, Identity, and Therapeutic Implications.

作者信息

Zou Nanyu, Liu Ran, Li Changjun

机构信息

Department of Endocrinology, Endocrinology Research Center, The Xiangya Hospital of Central South University, Changsha, China.

National Clinical Research Center for Geriatric Disorders (Xiangya Hospital), Changsha, China.

出版信息

Front Cell Dev Biol. 2022 Jul 13;10:818462. doi: 10.3389/fcell.2022.818462. eCollection 2022.

DOI:10.3389/fcell.2022.818462
PMID:35912093
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9326176/
Abstract

Cathepsin K (Ctsk) is a cysteine protease of the papain superfamily initially identified in differentiated osteoclasts; it plays a critical role in degrading the bone matrix. However, subsequent and studies based on animal models elucidate novel subpopulations of Ctsk-expressing cells, which display markers and properties of mesenchymal stem/progenitor cells. This review introduces the function, identity, and role of Ctsk cells and their therapeutic implications in related preclinical osseous disorder models. It also summarizes the available models for studying Ctsk cells and their progeny. Further investigations of detailed properties and mechanisms of Ctsk cells in transgenic models are required to guide potential therapeutic targets in multiple diseases in the future.

摘要

组织蛋白酶K(Ctsk)是木瓜蛋白酶超家族的一种半胱氨酸蛋白酶,最初在分化的破骨细胞中被鉴定出来;它在降解骨基质中起关键作用。然而,随后基于动物模型的研究阐明了表达Ctsk的细胞的新亚群,这些细胞表现出间充质干/祖细胞的标志物和特性。本综述介绍了Ctsk细胞的功能、特性和作用及其在相关临床前骨疾病模型中的治疗意义。它还总结了用于研究Ctsk细胞及其后代的现有模型。未来需要在转基因模型中进一步研究Ctsk细胞的详细特性和机制,以指导多种疾病的潜在治疗靶点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9719/9326176/5116aed664c7/fcell-10-818462-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9719/9326176/fc074d0a4d6d/fcell-10-818462-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9719/9326176/5116aed664c7/fcell-10-818462-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9719/9326176/fc074d0a4d6d/fcell-10-818462-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9719/9326176/5116aed664c7/fcell-10-818462-g002.jpg

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2
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Associations of Serum Cathepsin K and Polymorphisms in Gene With Bone Mineral Density and Bone Metabolism Markers in Postmenopausal Chinese Women.
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Mol Biotechnol. 2025 May;67(5):2085-2097. doi: 10.1007/s12033-024-01185-8. Epub 2024 May 23.
4
Mechanosensitive protein polycystin-1 promotes periosteal stem/progenitor cells osteochondral differentiation in fracture healing.机械敏感蛋白多囊蛋白-1促进骨折愈合过程中骨膜干/祖细胞的骨软骨分化。
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Age-related secretion of grancalcin by macrophages induces skeletal stem/progenitor cell senescence during fracture healing.年龄相关的巨噬细胞分泌钙粒蛋白诱导骨折愈合过程中骨骼干细胞/祖细胞衰老。
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