靶向炎症控制组织纤维化

Weihua Song, Wu Sun, Zilong Wang, K. Teo, C. Cheung, Xiaomeng Wang
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引用次数: 1

摘要

综述:靶向炎症控制组织纤维化宋卫华1,孙武2,王子龙3,易创创2,4,5,张翠明2,4,5,王晓梦4,5,*1创兰生物科技有限公司,江苏太仓215400北京西路6号;2新加坡国立眼科中心,新加坡第三医院大道168751号;3中国海洋大学,山东青岛市市南区玉山路5号;4新加坡眼科研究所,学院路169856号;5 Duke-NUS研究生医学院,20 College Road 169856,新加坡。6分子与细胞生物学研究所,61 Biopolis Dr, Proteos 138673,新加坡。摘要:细胞外基质(extracellular matrix, ECM)的重塑是宿主防御病原体和损伤后组织修复的重要过程。然而,异常的炎症反应可能会扰乱ECM稳态,导致组织结构和器官功能的进行性破坏。纤维化是多种疾病,特别是慢性炎症性疾病的常见结果,是全球发病率和死亡率的主要原因。这篇综述提供了目前对纤维化发病机制的理解,特别强调炎症在这一过程中的作用,以及靶向炎症作为控制纤维化进展策略的转化潜力。
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Targeting Inflammation to Control Tissue Fibrosis
Review Targeting Inflammation to Control Tissue Fibrosis Weihua Song 1, Wu Sun 2, Zilong Wang 3, Kelvin Yi Chong Teo 2,4,5, Chui Ming Gemmy Cheung 2,4,5, and Xiaomeng Wang 4,5,6,* 1 Innoland Biosciences, 6 West Beijing Road, Taicang 215400, Jiangsu, China. 2 Singapore National Eye Center, 11 Third Hospital Ave 168751, Singapore. 3 Ocean University of China, 5 Yushan Rd, Shinan District, Qingdao 266005, Shandong, China. 4 Singapore Eye Research Institute, 20 College Road 169856, Singapore. 5 Duke-NUS Graduate Medical School, 20 College Road 169856, Singapore. 6 Insitute of Molecular and Cell Biology, 61 Biopolis Dr, Proteos 138673, Singapore. * Correspondence: xiaomeng.wang@duke-nus.edu.sg     Received: 17 November 2022 Accepted: 19 November 2022 Published: 21 December 2022   Abstract: Remodeling of the extracellular matrix (ECM) is an essential process in host defense against pathogens and tissue repair following injury. However, aberrant inflammatory responses could disturb ECM homeostasis leading to progressive disruption in tissue architecture and organ function. Fibrosis is the common outcome of a wide range of diseases, especially chronic inflammatory disorders, and represents the leading cause of morbidity and mortality globally. This review provides the current understanding of the pathogenesis of fibrosis, with particular emphasis on the role of inflammation in this process and the translational potential of targeting inflammation as a strategy to control fibrotic progression.
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