Knocking out USP7 attenuates cardiac fibrosis and endothelial-to-mesenchymal transition by destabilizing SMAD3 in mice with heart failure with preserved ejection fraction
Shuai Yuan, Zimu Wang, Shun Yao, Yanyan Wang, Zhonglei Xie, Jingfeng Wang, Xueting Yu, Yu Song, Xiaotong Cui, Jingmin Zhou, Junbo Ge
Abstract
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.
Topics & Concepts
Cardiac fibrosisEjection fractionHeart failureMesenchymal stem cellFibrosisCardiologyInternal medicineMedicinePathologyCardiac Structural Anomalies and RepairCardiovascular Function and Risk FactorsCardiac Fibrosis and Remodeling