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

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

  • J Cell Mol Med. 2021 Jan;25(2):1001-1011. doi: 10.1111/jcmm.16162.
Qiong Xu 1 Mingke Liu 1 Fangcheng Zhang 1 Xiaolin Liu 1 Sisi Ling 1 Xuke Chen 1 Jielei Gu 1 Wenchao Ou 1 Shiming Liu 1 Ningning Liu 1
Affiliations

Affiliation

  • 1 Guangzhou Institute of Cardiovascular Disease, Guangdong Key Laboratory of Vascular Diseases, State Key Laboratory of Respiratory Disease, The Second Affiliated Hospital, Guangzhou Medical University, Guangzhou, China.
Abstract

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.

Keywords

USP2; cardiac fibrosis; collagen; proliferation; β-catenin.

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