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Hypoxia Induces Mesenchymal Gene Expression in Renal Tubular Epithelial Cells: An in vitro Model of Kidney Transplant Fibrosis
Author(s) -
Stephanie Zell,
Roland Schmitt,
Sandra Witting,
Hans Kreipe,
Kais Hussein,
Jan U. Becker
Publication year - 2013
Publication title -
nephron extra
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.413
H-Index - 7
ISSN - 1664-5529
DOI - 10.1159/000351046
Subject(s) - transplantation , mesenchymal stem cell , downregulation and upregulation , biology , kidney , epithelial–mesenchymal transition , cancer research , hypoxia (environmental) , fibrosis , endocrinology , microbiology and biotechnology , medicine , chemistry , gene , biochemistry , organic chemistry , oxygen
The development of interstitial fibrosis and tubular atrophy is a common complication after kidney transplantation and is associated with reduced long-term outcome. The hallmark of tubulointerstitial fibrosis is an increase in extracellular matrix resulting from exaggerated activation of fibroblasts/myofibroblasts, and tubular atrophy is characterized by a decrease in tubular diameter and loss of function. Atrophic epithelial cells may undergo epithelial-to-mesenchymal transition (EMT) with potential differentiation into interstitial fibroblasts. One potential driver of EMT in developing interstitial fibrosis and tubular atrophy is chronic hypoxia.

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