纤维化
发病机制
肾
医学
转化生长因子
炎症
肾脏疾病
癌症研究
免疫学
病理
内科学
作者
Yue-Yu Gu,Xusheng Liu,Xiao‐Ru Huang,Xueqing Yu,Hui Y. Lan
标识
DOI:10.4155/fmc-2020-0005
摘要
Renal fibrosis is a hallmark of chronic kidney disease. Although considerable achievements in the pathogenesis of renal fibrosis have been made, the underlying mechanisms of renal fibrosis remain largely to be explored. Now we have reached the consensus that TGF-β is a master regulator of renal fibrosis. Indeed, TGF-β regulates renal fibrosis via both canonical and noncanonical TGF-β signaling. Moreover, ongoing renal inflammation promotes fibrosis as inflammatory cells such as macrophages, conventional T cells and mucosal-associated invariant T cells may directly or indirectly contribute to renal fibrosis, which is also tightly regulated by TGF-β. However, anti-TGF-β treatment for renal fibrosis remains ineffective and nonspecific. Thus, research into mechanisms and treatment of renal fibrosis remains highly challenging.
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