Key result
Aldosterone increased ERK1/2 phosphorylation, alpha-SMA, and collagen III and IV expression in human renal proximal tubular epithelial cells, which was prevented by U0126 or spironolactone.
Aldosterone promotes tubulointerstitial fibrosis by inducing tubular epithelial-mesenchymal transition and collagen synthesis via an MR-dependent, ERK1/2-mediated pathway.
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Provides mechanistic insight into aldosterone-driven renal fibrosis in vitro; hypothesis-generating and should not change clinical practice.
Xu et al. (2008) studied Renal fibrosis. Aldosterone was evaluated on ERK1/2 phosphorylation, alpha-SMA, collagen III and IV, and E-cadherin expression. Aldosterone increased ERK1/2 phosphorylation, alpha-SMA, and collagen III and IV expression in human renal proximal tubular epithelial cells, which was prevented by U0126 or spironolactone.
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