New Insights into Epithelial-Mesenchymal Transition in Kidney Fibrosis

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...

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Bibliographic Details
Published in:Journal of the American Society of Nephrology 2010-02, Vol.21 (2), p.212-222
Main Author: Liu, Youhua
Format: Article
Language:English
Subjects:
Biological and medical sciences
Cell Differentiation
Epithelial Cells - pathology
Fibrosis
Humans
Kidney - pathology
Kidneys
Medical sciences
Mesoderm - pathology
Nephrology. Urinary tract diseases
Podocytes - pathology
Signal Transduction
Urinary system involvement in other diseases. Miscellaneous
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Summary: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.
ISSN:1046-6673
1533-3450
DOI:10.1681/ASN.2008121226