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Veerasamy M et al. – The results suggest that E–cadherin loss, the key feature of EMT will not necessarily be followed by total phenotype change; rather cells may undergo some loss of phenotypic marker in a ligand dependent manner and participate in reparative processes. The inhibition of de novo expression of alpha–SMA could explain the anti–fibrotic effect of BMP 7. Id1 might play a crucial role in maintaining PTEC phenotype and its signaling regulation could be a potential therapeutic target.

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