Epithelial-to-Mesenchymal Transition in Diabetic Nephropathy: Fact or Fiction?

Cells

Ivonne Loeffler²  Gunter Wolf¹ 

[1] id="af1-cells-04-00631">Department of Internal Medicine III, University Hospital, University of Jena, Erlanger Allee 101, D-07747 Jena, Germa

关键词: epithelial-to-mesenchymal transition (EMT);    endothelial-to-mesenchymal transition (EndoMT);    diabetic nephropathy;    renal fibrosis;   

DOI  :  10.3390/cells4040631

来源: mdpi

【 摘 要 】

The pathophysiology of diabetic nephropathy (DN), one of the most serious complications in diabetic patients and the leading cause of end-stage renal disease worldwide, is complex and not fully elucidated. A typical hallmark of DN is the excessive deposition of extracellular matrix (ECM) proteins in the glomerulus and in the renal tubulointerstitium, eventually leading to glomerulosclerosis and interstitial fibrosis. Although it is obvious that myofibroblasts play a major role in the synthesis and secretion of ECM, the origin of myofibroblasts in DN remains the subject of controversial debates. A number of studies have focused on epithelial-to-mesenchymal transition (EMT) as one source of matrix-generating fibroblasts in the diseased kidney. EMT is characterized by the acquisition of mesenchymal properties by epithelial cells, preferentially proximal tubular cells and podocytes. In this review we comprehensively review the literature and discuss arguments both for and against a function of EMT in renal fibrosis in DN. While the precise extent of the contribution to nephrotic fibrosis is certainly arduous to quantify, the picture that emerges from this extensive body of literature suggests EMT as a major source of myofibroblasts in DN.

【 授权许可】

CC BY   
© 2015 by the authors; licensee MDPI, Basel, Switzerland.