Key result
Atorvastatin inhibits TGF-beta1-induced endoglin and collagen I expression in cardiac fibroblasts through the inhibition of PI-3 kinase, Akt, and Smad3 phosphorylation.
Atorvastatin attenuates cardiac fibrosis by inhibiting TGF-beta1-induced endoglin expression via the PI-3 kinase/Akt and Smad3 signaling pathways.
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Hypothesis-generating for statin effects on cardiac fibrosis; leaves open translation from fibroblasts to in vivo models or patients.
Shyu et al. (2010) studied Cardiac fibrosis. Atorvastatin vs. Control / TGF-beta1 stimulation alone was evaluated on Endoglin and collagen I expression, PI-3 kinase/Akt phosphorylation, and Smad3/4 binding activity. Atorvastatin inhibits TGF-beta1-induced endoglin and collagen I expression in cardiac fibroblasts through the inhibition of PI-3 kinase, Akt, and Smad3 phosphorylation.
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