Amelioration of Endothelial Dysfunction in Diabetes: Role of Takeda G Protein-Coupled Receptor 5

Zhengyao Cai; Suxin Yuan; Yi Zhong; Li Deng; Jiafu Li; Xiaoqiu Tan; Jian Feng

doi:10.3389/fphar.2021.637051

Amelioration of Endothelial Dysfunction in Diabetes: Role of Takeda G Protein-Coupled Receptor 5

Front Pharmacol. 2021 Apr 28:12:637051. doi: 10.3389/fphar.2021.637051. eCollection 2021.

Authors

Zhengyao Cai¹, Suxin Yuan¹, Yi Zhong¹, Li Deng², Jiafu Li¹, Xiaoqiu Tan¹, Jian Feng¹

Affiliations

¹ Department of Cardiology, The Affiliated Hospital of Southwest Medical University, Key Laboratory of Medical Electrophysiology, Ministry of Education and Medical Electrophysiological Key Laboratory of Sichuan Province, Institute of Cardiovascular Research, Southwest Medical University, Luzhou, China.
² Department of Rheumatology, The Affiliated Hospital of Southwest Medical University, Luzhou, China.

Abstract

Diabetes mellitus (DM) eventually leads to chronic vascular complications, resulting in cardiovascular diseases. DM-associated endothelial dysfunction (ED) plays an important role in the development of chronic vascular complications. Low endothelial nitric oxide synthase (eNOS) activity, inflammation, and oxidative stress all contribute to ED. The G protein-coupled receptor Takeda G protein-coupled receptor 5 (TGR5) is a membrane receptor for bile acids that plays an important role in the regulation of glucose metabolism. Recent studies have shown that TGR5 is involved in the regulation of various mediators of ED, which suggests that TGR5 may represent a target for the treatment of DM-associated ED. In this review, we summarize the principal mechanisms of DM-associated ED, then propose TGR5 as a novel therapeutic target on the basis of its mechanistic involvement, and suggest potential directions for future research.

Keywords: TGR5; diabetes mellitus; endothelial dysfunction; endothelial nitric oxide synthase; inflammation; oxidative stress.

Publication types

Review