Epithelial to mesenchymal transition in the progression of tubulointerstitial fibrosis.
OBJECTIVE
To review the mechanisms of epithelial to mesenchymal transition (EMT) and its role in the progression of tubulointerstitial fibrosis.


METHODS
The data used in this review were obtained mainly from the studies of EMT reported from 2000-2006.


METHODS
Relevant articles on studies of EMT in tubulointerstitial fibrosis were selected. Data were mainly extracted from the 45 articles listed in the reference section of this review.


RESULTS
The process of EMT has gained wide recognition as candidate mechanism in progression of chronic fibrotic disorders. New markers were identified and facilitate the observation of EMT. EMT is regulated by many factors through activation of kinase-dependent signaling cascades. Recent findings suggest that EMT is a reversible process, which can be controlled by factors for their epithelial inducing activities.


CONCLUSIONS
Remarkable progresses of EMT research have been made recently. Preventing or reversing EMT is a promising strategy against renal fibrosis.
Li
Min-xia
MX
Institute of Nephrology, Zhong Da Hospital, Southeast University, Nanjing, China.
Liu
Bi-cheng
BC
D000818:Animals; D055513:Connective Tissue Growth Factor; D018450:Disease Progression; D004848:Epithelium / Q000378:metabolism / Q000473:pathology*; D005355:Fibrosis; D006801:Humans; D017874:Immediate-Early Proteins / Q000378:metabolism; D036341:Intercellular Signaling Peptides and Proteins / Q000378:metabolism; D008648:Mesoderm / Q000378:metabolism / Q000473:pathology*; D009395:Nephritis, Interstitial / Q000378:metabolism / Q000473:pathology*; D015291:Transforming Growth Factors / Q000378:metabolism
C526317:CCN2 protein, human; D017874:Immediate-Early Proteins; D036341:Intercellular Signaling Peptides and Proteins; D055513:Connective Tissue Growth Factor; D015291:Transforming Growth Factors