Does knocking out USP7 attenuate cardiac fibrosis and endothelial-to-mesenchymal transition in mice with heart failure with preserved ejection fraction?
USP7 knockout attenuates cardiac fibrosis and endothelial-to-mesenchymal transition in a mouse model of HFpEF, suggesting USP7 and SMAD3 as potential therapeutic targets.
Our results indicated that USP7 is one of the key pathogenic molecules of HFpEF, and knocking out USP7 could attenuate HFpEF injury by promoting the degradation of SMAD3. USP7 and SMAD3 inhibition might be potential therapeutic options for HFpEF.
Yuan et al. (Mon,) studied this question.