TGF-β/Smad and Renal Fibrosis
Renal fibrosis is characterized by excessive deposition of extracellular matrix (ECM) that disrupts and replaces functional parenchyma, which leads to organ failure. It is known as the major pathological mechanism of chronic kidney disease (CKD). Although CKD has an impact on no less than 10% of the world population, therapeutic options are still limited. Regardless of etiology, elevated TGF-β levels are highly correlated with the activated pro-fibrotic pathways and disease progression. TGF-β, the key driver of renal fibrosis, is involved in a dynamic pathophysiological process that leads to CKD and end-stage renal disease (ESRD). It is becoming clear that epigenetics regulates renal programming, and therefore, the development and progression of renal disease. Indeed, recent evidence shows TGF-β1/Smad signaling regulates renal fibrosis via epigenetic-correlated mechanisms. This review focuses on the function of TGF-β/Smads in renal fibrogenesis, and the role of epigenetics as a regulator of pro-fibrotic gene expression.
KeywordsTGF-β Renal fibrosis Smad Non-coding RNA Epigenetic modification
The laboratory is supported by grants from National Natural Science Foundation of China (National Science Foundation of China 81300580 and 81570623), and by Science and Technological Fund of Anhui Province for Outstanding Youth of China (Grant number: 1608085J07)
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