足细胞
上皮-间质转换
纤维化
肾小球硬化
Wnt信号通路
癌症研究
SMAD公司
肌成纤维细胞
信号转导
细胞生物学
局灶节段性肾小球硬化
背景(考古学)
生物
病理
肾
医学
肾小球肾炎
内科学
内分泌学
蛋白尿
癌症
古生物学
转移
出处
期刊:Journal of The American Society of Nephrology
日期:2010-02-01
卷期号:21 (2): 212-222
被引量:760
标识
DOI:10.1681/asn.2008121226
摘要
Epithelial-mesenchymal transition (EMT), a process by which differentiated epithelial cells undergo a phenotypic conversion that gives rise to the matrix-producing fibroblasts and myofibroblasts, is increasingly recognized as an integral part of tissue fibrogenesis after injury. However, the degree to which this process contributes to kidney fibrosis remains a matter of intense debate and is likely to be context-dependent. EMT is often preceded by and closely associated with chronic interstitial inflammation and could be an adaptive response of epithelial cells to a hostile or changing microenvironment. In addition to tubular epithelial cells, recent studies indicate that endothelial cells and glomerular podocytes may also undergo transition after injury. Phenotypic alteration of podocytes sets them in motion to functional impairment, resulting in proteinuria and glomerulosclerosis. Several intracellular signal transduction pathways such as TGFbeta/Smad, integrin-linked kinase (ILK) and Wnt/beta-catenin signaling are essential in controlling the process of EMT and presently are potential targets of antifibrotic therapy. This review highlights the current understanding of EMT and its underlying mechanisms to stimulate further discussion on its role, not only in the pathogenesis of renal interstitial fibrosis but also in the onset of podocyte dysfunction, proteinuria, and glomerulosclerosis.
科研通智能强力驱动
Strongly Powered by AbleSci AI