纤维细胞
基质金属蛋白酶
细胞外基质
医学
基质金属蛋白酶抑制剂
特发性肺纤维化
纤维化
癌症研究
肺纤维化
基因沉默
免疫学
肺
内科学
细胞生物学
病理
生物
化学
生物化学
基因
作者
Sushweta Mahalanobish,Sukanya Saha,Sayanta Dutta,Parames C. Sil
标识
DOI:10.1016/j.phrs.2019.104591
摘要
Idiopathic pulmonary fibrosis (IPF) is a debilitating condition where excess collagen deposition occurs in the extracellular matrix. At first sight, it is expected that the level of different kinds of matrix metalloproteinases might be downregulated in IPF as it is a matrix degrading collagenase. However, the role of some matrix metalloproteinases (MMPs) is profibrotic where others have anti-fibrotic functions. These profibrotic MMPs effectively promote fibrosis development by stimulating the process of epithelial to mesenchymal transition. These profibrotic groups also induce macrophage polarization and fibrocyte migration. All of these events ultimately disrupt the balance between profibrotic and antifibrotic mediators, resulting aberrant repair process. Therefore, inhibition of these matrix metalloproteinases functions in IPF is a potential therapeutic approach. In addition to the use of synthetic inhibitor, various natural compounds, gene silencing act as potential natural MMP inhibitor to recover IPF.
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