Partial Epithelial-to-Mesenchymal Transition and Other New Mechanisms of Kidney Fibrosis

被引：211

作者：

Lovisa, Sara ^{[1
]}

Zeisberg, Michael ^{[2
]}

Kalluri, Raghu ^{[1
,3
,4
]}

机构：

[1] Univ Texas MD Anderson Canc Ctr, Metastasis Res Ctr, Dept Canc Biol, Houston, TX 77054 USA

[2] Univ Gottingen, Med Ctr, Dept Nephrol & Rheumatol, Gottingen, Germany

[3] Baylor Coll Med, Dept Mol & Cellular Biol, Houston, TX 77030 USA

[4] Rice Univ, Dept Bioengn, Houston, TX 77030 USA

来源：

TRENDS IN ENDOCRINOLOGY AND METABOLISM | 2016年 / 27卷 / 10期

关键词：

CELL-CYCLE ARREST; PERICYTE-MYOFIBROBLAST TRANSITION; RENAL FIBROSIS; GROWTH-FACTOR; PROXIMAL TUBULE; FIBROBLAST ACTIVATION; EXPERIMENTAL GLOMERULONEPHRITIS; MITOCHONDRIAL DYSFUNCTION; LIPID-ACCUMULATION; MAMMALIAN TARGET;

D O I：

10.1016/j.tem.2016.06.004

中图分类号：

R5 [内科学];

学科分类号：

1002 ; 100201 ;

摘要：

Kidney fibrosis is the unavoidable consequence of chronic kidney disease irrespective of the primary underlying insult. It is a complex phenomenon governed by the interplay between different cellular components and intricate networks of signaling pathways, which together lead to loss of renal functionality and replacement of kidney parenchyma with scar tissue. An immense effort has recently been made to understand the molecular and cellular mechanisms leading to kidney fibrosis. The cellular protagonists of this process include myofibroblasts, tubular epithelial cells, endothelial cells, and immune cells. We discuss here the most recent findings, including partial epithelial-to-mesenchymal transition (EMT), in the initiation and progression of tissue fibrosis and chronic kidney disease (CKD). A deep understanding of these mechanisms will allow the development of effective therapies.

引用

页码：681 / 695

页数：15

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