Abstract
Snail family zinc finger 1 (SNAI1) is a transcription factor expressed during renal embryogenesis, and re-expressed in various settings of acute kidney injury (AKI). Subjected to tight regulation, SNAI1 controls major biological processes responsible for renal fibrogenesis, including mesenchymal reprogramming of tubular epithelial cells, shutdown of fatty acid metabolism, cell cycle arrest and inflammation of the microenvironment surrounding tubular epithelial cells. The present review describes in detail the interactions of SNAI1 with AKI-associated signalling pathways. We also discuss how this central factor has been iteratively (and promisingly) targeted in a number of animal models in order to prevent or slow down renal fibrogenesis.
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