Knocking out USP7 attenuates cardiac fibrosis and endothelial-to-mesenchymal transition by destabilizing SMAD3 in mice with heart failure with preserved ejection fraction

• Published in: Theranostics Vol. 14; no. 15; pp. 5793 - 5808
• Main Authors: Yuan, Shuai, Wang, Zimu, Yao, Shun, Wang, Yanyan, Xie, Zhonglei, Wang, Jingfeng, Yu, Xueting, Song, Yu, Cui, Xiaotong, Zhou, Jingmin, Ge, Junbo
• Format: Journal Article
• Language: English
• Published: Australia Ivyspring International Publisher 01.01.2024
• Subjects: Animals; Disease Models, Animal; Epithelial-Mesenchymal Transition - genetics; Female; Fibrosis - metabolism; Heart Failure - genetics; Heart Failure - metabolism; Humans; Mice; Mice, Inbred C57BL; Mice, Knockout; Myocardium - metabolism; Myocardium - pathology; Research Paper; Smad3 Protein - metabolism; Stroke Volume; Ubiquitin-Specific Peptidase 7 - genetics; Ubiquitin-Specific Peptidase 7 - metabolism; Heart failure with preserved ejection fraction; Cardiac fibrosis; USP7; Endothelial-to-mesenchymal transition; Deubiquitination enzyme

: Heart failure with preserved ejection fraction (HFpEF) is a predominant type of heart failure. Exploring new pathogenesis and identifying potential novel therapeutic targets for HFpEF is of paramount importance. : HFpEF mouse model was established by the "Multiple-hit" strategy, in that...