Targeting ADAMTS1 and HDAC6 with specific inhibitors or shRNA alleviated TGF-β1/SMAD2-associated myocardial fibrosis and improved cardiac function in a mouse model of post-myocardial infarction.
Does targeting ADAMTS1/HDAC6 reduce myocardial fibrosis and improve cardiac function in post-myocardial infarction models?
Inhibition of ADAMTS1 or HDAC6 attenuates TGF-β1/SMAD2-mediated cardiac fibrosis and improves cardiac function in post-myocardial infarction models.
Targeting ADAMTS1/HDAC6 alleviated TGF-β1/SMAD2-associated cardiac fibrosis in CFPMI. This study may provide a novel theoretical basis for the treatment of myocardial fibrosis.
Jin et al. (Thu,) conducted a other in Cardiac fibrosis post-myocardial infarction (n=60). ADAMTS1 inhibitor and shRNA-HDAC6 vs. Sham or CFPMI with control AAV was evaluated on Myocardial fibrosis and cardiac function. Targeting ADAMTS1 and HDAC6 with specific inhibitors or shRNA alleviated TGF-β1/SMAD2-associated myocardial fibrosis and improved cardiac function in a mouse model of post-myocardial infarction.