Next Article in Journal
Active Nuclear Import of Membrane Proteins Revisited
Next Article in Special Issue
Role of the Polycystins in Cell Migration, Polarity, and Tissue Morphogenesis
Previous Article in Journal / Special Issue
Albumin and Furosemide Combination for Management of Edema in Nephrotic Syndrome: A Review of Clinical Studies
Article Menu

Export Article

Open AccessReview
Cells 2015, 4(4), 631-652; doi:10.3390/cells4040631

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

Department of Internal Medicine III, University Hospital, University of Jena, Erlanger Allee 101, D-07747 Jena, Germany
Author to whom correspondence should be addressed.
Academic Editor: Christoph Englert
Received: 28 August 2015 / Revised: 29 September 2015 / Accepted: 30 September 2015 / Published: 9 October 2015
(This article belongs to the Special Issue The Kidney: Development, Disease and Regeneration)
View Full-Text   |   Download PDF [1384 KB, uploaded 9 October 2015]   |  


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. View Full-Text
Keywords: epithelial-to-mesenchymal transition (EMT); endothelial-to-mesenchymal transition (EndoMT); diabetic nephropathy; renal fibrosis epithelial-to-mesenchymal transition (EMT); endothelial-to-mesenchymal transition (EndoMT); diabetic nephropathy; renal fibrosis

Figure 1

This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. (CC BY 4.0).

Scifeed alert for new publications

Never miss any articles matching your research from any publisher
  • Get alerts for new papers matching your research
  • Find out the new papers from selected authors
  • Updated daily for 49'000+ journals and 6000+ publishers
  • Define your Scifeed now

SciFeed Share & Cite This Article

MDPI and ACS Style

Loeffler, I.; Wolf, G. Epithelial-to-Mesenchymal Transition in Diabetic Nephropathy: Fact or Fiction? Cells 2015, 4, 631-652.

Show more citation formats Show less citations formats

Related Articles

Article Metrics

Article Access Statistics



[Return to top]
Cells EISSN 2073-4409 Published by MDPI AG, Basel, Switzerland RSS E-Mail Table of Contents Alert
Back to Top