Key result
Overexpression of human ACE in the myocardium of transgenic rats increased myocardial collagen content up to 2.5-fold (P<0.01) by degrading AcSDKP and increasing Smad2/3 phosphorylation.
Why the study?
Does ACE inhibition or AcSDKP infusion reduce myocardial collagen content and Smad2/3 phosphorylation in transgenic rats overexpressing cardiac ACE?
Does ACE inhibition or AcSDKP infusion reduce myocardial collagen content and Smad2/3 phosphorylation in transgenic rats overexpressing cardiac ACE?
Effect estimate: up to 2.5-fold increase
p-value: p=<0.01
Increased cardiac ACE activity promotes myocardial fibrosis by degrading the antifibrotic peptide AcSDKP, leading to increased Smad2/3 phosphorylation, a process reversible by ACE inhibitors.
No takes yet. Share an insight, caveat, or question.
ACE inhibition reverses experimental myocardial fibrosis in rats; leaves open human translation of AcSDKP-Smad pathways.
Pokharel et al. (2004) studied Myocardial fibrosis. Overexpression of human ACE vs. Control rats was evaluated on Myocardial collagen content (up to 2.5-fold increase, p=<0.01). Overexpression of human ACE in the myocardium of transgenic rats increased myocardial collagen content up to 2.5-fold (P<0.01) by degrading AcSDKP and increasing Smad2/3 phosphorylation.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: