Epithelial-to-Mesenchymal Transition in Diabetic Nephropathy: Fact or Fiction?
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...
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| Format: | Online |
| Language: | English |
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MDPI
2015
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| Online Access: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4695850/ |
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pubmed-4695850 |
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pubmed-46958502016-01-19 Epithelial-to-Mesenchymal Transition in Diabetic Nephropathy: Fact or Fiction? Loeffler, Ivonne Wolf, Gunter Review 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. MDPI 2015-10-09 /pmc/articles/PMC4695850/ /pubmed/26473930 http://dx.doi.org/10.3390/cells4040631 Text en © 2015 by the authors; licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution license (http://creativecommons.org/licenses/by/4.0/). |
| repository_type |
Open Access Journal |
| institution_category |
Foreign Institution |
| institution |
US National Center for Biotechnology Information |
| building |
NCBI PubMed |
| collection |
Online Access |
| language |
English |
| format |
Online |
| author |
Loeffler, Ivonne Wolf, Gunter |
| spellingShingle |
Loeffler, Ivonne Wolf, Gunter Epithelial-to-Mesenchymal Transition in Diabetic Nephropathy: Fact or Fiction? |
| author_facet |
Loeffler, Ivonne Wolf, Gunter |
| author_sort |
Loeffler, Ivonne |
| title |
Epithelial-to-Mesenchymal Transition in Diabetic Nephropathy: Fact or Fiction? |
| title_short |
Epithelial-to-Mesenchymal Transition in Diabetic Nephropathy: Fact or Fiction? |
| title_full |
Epithelial-to-Mesenchymal Transition in Diabetic Nephropathy: Fact or Fiction? |
| title_fullStr |
Epithelial-to-Mesenchymal Transition in Diabetic Nephropathy: Fact or Fiction? |
| title_full_unstemmed |
Epithelial-to-Mesenchymal Transition in Diabetic Nephropathy: Fact or Fiction? |
| title_sort |
epithelial-to-mesenchymal transition in diabetic nephropathy: fact or fiction? |
| description |
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. |
| publisher |
MDPI |
| publishDate |
2015 |
| url |
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4695850/ |
| _version_ |
1613518196250247168 |