Open AccessUbiquitin‐specific protease 2 regulates Ang Ⅱ–induced cardiac fibroblasts activation by up‐regulating cyclin D1 and stabilizing β‐catenin in vitro
Author(s) -
Xu Qiong,
Liu Mingke,
Zhang Fangcheng,
Liu Xiaolin,
Ling Sisi,
Chen Xuke,
Gu Jielei,
Ou Wenchao,
Liu Shiming,
Liu Ningning
Publication year - 2021
Publication title -
journal of cellular and molecular medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.44
H-Index - 130
eISSN - 1582-4934
pISSN - 1582-1838
DOI - 10.1111/jcmm.16162
Subject(s) - cardiac fibrosis , myocardial fibrosis , cardiac function curve , fibrosis , cancer research , ubiquitin , angiotensin ii , extracellular matrix , cyclin d1 , chemistry , microbiology and biotechnology , catenin , heart failure , cell cycle , medicine , wnt signaling pathway , biology , signal transduction , cell , biochemistry , receptor , gene
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.