Abstract
Our current understanding of epithelial-mesenchymal transition (EMT) in the setting of tissue fibrosis is largely based on pioneering studies in the kidney. Evidence is emerging that EMT is a key component of chronic kidney disease, contributing to both destruction of the tubular epithelial compartment and accumulation of interstitial fibroblasts. While knowledge regarding EMT was previously based on experimental rodent studies, in recent years the evolving evidence demonstrates a role for EMT in human kidney diseases with chronic fibrosis.
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