The mechanosensitive APJ internalization via clathrin-mediated endocytosis: A new molecular mechanism of cardiac hypertrophy

被引：16

作者：

He, Lu ^{[1
]}

Chen, Linxi ^{[1
]}

Li, Lanfang ^{[1
]}

机构：

[1] Univ South China, Hunan Prov Cooperat Innovat Ctr Mol Target New Dr, Inst Pharm & Pharmacol, Learning Key Lab Pharmacoprote, Hengyang 421001, Peoples R China

来源：

MEDICAL HYPOTHESES | 2016年 / 90卷

基金：

中国国家自然科学基金; 中国博士后科学基金;

关键词：

APELIN RECEPTOR AGONIST; HEART-FAILURE; HYPERTENSION; CELLS; PRESSURE; PATHWAY; CARDIOMYOPATHY; IDENTIFICATION; NEUROPEPTIDE; ACTIVATION;

D O I：

10.1016/j.mehy.2016.02.017

中图分类号：

R-3 [医学研究方法]; R3 [基础医学];

学科分类号：

1001 ;

摘要：

The G protein-coupled receptor APJ elicits cellular response to diverse extracellular stimulus. Accumulating evidence reveals that APJ receptor plays a prominent role in the cardiomyocyte adapting to hypertrophic stimulation. At present, it remains obscure that the regulatory mechanism of APJ receptor in myocardial hypertrophy. The natural endogenous ligands apelin and Elabela as well as agonists maintain high affinity for the APJ receptor and drive its internalization. Ligand-activated receptor internalization is mainly performed by clathrin-mediated endocytic pathway. Simultaneously, clathrin-mediated endocytosis takes participate in the occurrence and development of cardiac hypertrophy. In this study, we hypothesize that natural ligands and agonists induce the mechanosensitive APJ internalization via clathrin-mediated endocytosis. APJ internalization may contribute to the development of cardiac hypertrophy. The mechanosensitive APJ internalization via clathrin-mediated endocytosis may be a new molecular mechanism of cardiac hypertrophy. (C) 2016 Elsevier Ltd. All rights reserved.

引用

页码：6 / 10

页数：5

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