Cardiac fibroblast heat shock protein 47 aggravates cardiac fibrosis post myocardial ischemia–reperfusion injury by encouraging ubiquitin specific peptidase 10 dependent Smad4 deubiquitination
Saiyang Xie, Yun Xing, Wenke Shi, Min Zhang, Mengya Chen, Wenxi Fang, Shiqiang Liu, Tong Zhang, Xiaofeng Zeng, Si Chen, Shasha Wang, Wei Deng, Qi‐Zhu Tang
Abstract
1-Smad4 pathway activation and Smad4 deubiquitination by recruiting ubiquitin-specific peptidase 10 (USP10) in fibroblasts. However, cardiac fibroblast specific USP10 deficiency abolished HSP47-mediated fibrogenesis in hearts. Moreover, blockage of HSP47 with Col003 disturbed fibrogenesis in fibroblasts following HR. Altogether, cardiac fibroblast HSP47 aggravates fibrosis post-myocardial IRI by enhancing USP10-dependent Smad4 deubiquitination, which provided a potential strategy for myocardial IRI and cardiac remodeling.
Topics & Concepts
Cardiac fibrosisMedicineReperfusion injuryMyocardial infarctionFibrosisMyocardial fibrosisIschemiaFibroblastCardiologyPercutaneous coronary interventionInternal medicineBiologyBiochemistryIn vitroCardiac Fibrosis and RemodelingCardiovascular Function and Risk FactorsCardiac Ischemia and Reperfusion