脱落的Syndecan-4及其在骨关节炎中的可能作用。
Shed Syndecan-4 and Its Possible Roles in Osteoarthritis.
作者信息
He Kangping, Ren Haozhe, Chen Xiaohua, He Feng, Zhang Yueying, Zhang Hongyun, Li Feifei, Yu Shibin
机构信息
State Key Laboratory of Oral & Maxillofacial Reconstruction and Regeneration, National Clinical Research Center for Oral Diseases, Shaanxi International Joint Research Center for Oral Diseases, School of Stomatology, The Fourth Military Medical University, Xi'an 710032, China.
School/Hospital of Stomatology, Lanzhou University, Lanzhou 730000, China.
出版信息
Biomedicines. 2025 Apr 25;13(5):1037. doi: 10.3390/biomedicines13051037.
The specific pathogenesis of osteoarthritis (OA) remains not fully understood. As a transmembrane heparan sulfate proteoglycan, syndecan-4 (SDC4) has been proven to play an important role in the development of OA. Notably, the extracellular domain of SDC4 can be cleaved by proteolytic enzymes, leading to the release of shed SDC4 (sSDC4), which subsequently regulates various biological processes in an autocrine or paracrine manner. This review analyzed 97 publications (1987-2025) from Pubmed and the Web of Science Core Collection using specific key words (syndecan-4, shed syndecan-4, and osteoarthritis), providing a comprehensive overview of the current research on sSDC4, including its shedding enzymes and specific cleavage sites, as well as the factors and mechanisms that influence SDC4 shedding. Furthermore, it summarizes the functions of both sSDC4 and its remaining membrane-bound domain. Finally, the roles of sSDC4 in OA are discussed to identify potential therapeutic targets and explore new strategies for the treatment of OA.
骨关节炎（OA）的具体发病机制仍未完全明确。作为一种跨膜硫酸乙酰肝素蛋白聚糖，Syndecan-4（SDC4）已被证明在OA的发展中起重要作用。值得注意的是，SDC4的细胞外结构域可被蛋白水解酶切割，导致脱落的SDC4（sSDC4）释放，随后sSDC4以自分泌或旁分泌方式调节各种生物学过程。本综述使用特定关键词（Syndecan-4、脱落的Syndecan-4和骨关节炎）分析了来自PubMed和科学网核心合集的97篇出版物（1987 - 2025年），全面概述了目前关于sSDC4的研究，包括其脱落酶和特定切割位点，以及影响SDC4脱落的因素和机制。此外，还总结了sSDC4及其剩余膜结合结构域的功能。最后，讨论了sSDC4在OA中的作用，以确定潜在的治疗靶点并探索治疗OA的新策略。
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