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Ubiquitin‐specific protease 2 regulates Ang Ⅱ–induced cardiac fibroblasts activation by up‐regulating cyclin D1 and stabilizing β‐catenin in vitro

Cardiac fibrosis, featuring abnormally elevated extracellular matrix accumulation, decreases tissue compliance, impairs cardiac function and accelerates heart failure. Mounting evidence suggests that the ubiquitin proteasome pathway is involved in cardiac fibrosis. In the present study, ubiquitin‐sp...

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Detalles Bibliográficos
Autores principales: Xu, Qiong, Liu, Mingke, Zhang, Fangcheng, Liu, Xiaolin, Ling, Sisi, Chen, Xuke, Gu, Jielei, Ou, Wenchao, Liu, Shiming, Liu, Ningning
Formato: Online Artículo Texto
Lenguaje:English
Publicado: John Wiley and Sons Inc. 2020
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7812274/
https://www.ncbi.nlm.nih.gov/pubmed/33314748
http://dx.doi.org/10.1111/jcmm.16162
Descripción
Sumario:Cardiac fibrosis, featuring abnormally elevated extracellular matrix accumulation, decreases tissue compliance, impairs cardiac function and accelerates heart failure. Mounting evidence suggests that the ubiquitin proteasome pathway is involved in cardiac fibrosis. In the present study, ubiquitin‐specific protease 2 (USP2) was identified as a novel therapeutic target in cardiac fibrosis. Indeed, USP2 expression was increased in angiotensin II–induced primary cardiac fibroblasts (CFs) from neonatal rats. In addition, USP2 inhibition suppressed CFs proliferation, collagen synthesis and cell cycle progression. Furthermore, USP2 interacted with β‐catenin, thereby regulating its deubiquitination and stabilization in CFs. To sum up, these findings revealed that USP2 has a therapeutic potential for the treatment of cardiac fibrosis.