HIGHLIGHTS
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Exploring the role of TGFβ and its associate genes in the pathogenetic mechanism of EMT in renal fibrosis.
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Possible immunohistochemical markers (Pancytokeratin, SMA and Vimentin) to identify the process of EMT.
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Availability of various EMT related anti-fibrotic therapy with emphasis on stem cell therapy.
Abstract
Renal fibrosis in chronic renal failure poses a major challenge with regard to providing specific therapeutic strategies.
The current hypothesis of the epithelial-mesenchymal transition (EMT) in renal fibrosis proposes that matrix producing fibroblasts and myofibroblasts generated in the diseased kidney causes fibrosis. This paper explores the pathogenetic mechanisms, the role of EMT in renal fibrogenesis in chronic kidney disease, biomarkers, and EMT related anti-fibrotic therapy.
Keywords:
renal fibrosis; myofibroblast; epithelial-mesenchymal transition; chronic kidney disease; anti-fibrotic therapy.