Yan Suyan, Zhao Yaqi, Yang Yuyu, Liu Baocheng, Xu Wei, Ma Zhenzhen, Yang Qingrui
Department of Rheumatology and Immunology, Shandong Provincial Hospital Affiliated to Shandong First Medical University, Jinan 250021, Shandong, China.
Department of Rheumatology and Immunology, Shandong Provincial Hospital, Cheeloo College of Medicine, Shandong University, Jinan 250021, Shandong, China.
Mediators Inflamm. 2025 Feb 26;2025:9999723. doi: 10.1155/mi/9999723. eCollection 2025.
Fibrosis leads to structural damage and functional decline and is characterized by an accumulation of fibrous connective tissue and a reduction in parenchymal cells. Because of its extremely poor prognosis, organ fibrosis poses a significant economic burden. In order to prevent and treat fibrosis more effectively, potential mechanisms need to be investigated. A disintegrin and metalloprotease 17 (ADAM17) is a membrane-bound protein. It regulates intracellular signaling and membrane protein degradation. Fibrosis mediated by ADAM17 has been identified as an important contributor, although the specific relationship between its multiple regulatory functions and the pathogenesis is unclear. This article describes ADAM17 activation, function, and regulation, as well as the role of ADAM17 mediated fibrosis injury in kidney, liver, heart, lung, skin, endometrium, and retina. To develop new therapeutic approaches based on ADAM17 related signal pathways.
纤维化会导致结构损伤和功能衰退，其特征是纤维结缔组织的积累和实质细胞的减少。由于其预后极差，器官纤维化带来了巨大的经济负担。为了更有效地预防和治疗纤维化，需要研究其潜在机制。解整合素金属蛋白酶17（ADAM17）是一种膜结合蛋白。它调节细胞内信号传导和膜蛋白降解。尽管ADAM17的多种调节功能与发病机制之间的具体关系尚不清楚，但已确定ADAM17介导的纤维化是一个重要因素。本文描述了ADAM17的激活、功能和调节，以及ADAM17介导的纤维化损伤在肾脏、肝脏、心脏、肺、皮肤、子宫内膜和视网膜中的作用。旨在基于ADAM17相关信号通路开发新的治疗方法。
