Apelin/APJ system: A novel therapeutic target for oxidative stress-related inflammatory diseases (Review)

被引:72
作者
Zhou, Qun [1 ,2 ]
Cao, Jiangang [1 ]
Chen, Linxi [1 ]
机构
[1] Univ South China, Inst Pharm & Pharmacol, Learning Key Lab Pharmacoprote, 28 Changsheng Rd, Hengyang 421001, Hunan, Peoples R China
[2] Hunan Univ Med, Coll Pharm, Huaihua 418000, Hunan, Peoples R China
基金
中国博士后科学基金; 中国国家自然科学基金;
关键词
apelin; APJ; oxidative stress; reactive oxygen species; inflammation; atherosclerosis; hypertension; ischemia-reperfusion injury; MONOCYTE CHEMOATTRACTANT PROTEIN-1; SIGNALING TRANSDUCTION PATHWAY; MUSCLE-CELL PROLIFERATION; ORPHAN RECEPTOR APJ; ISOLATED RAT HEARTS; CANCER STEM-CELLS; NF-KAPPA-B; NITRIC-OXIDE; DIABETIC-NEPHROPATHY; ISCHEMIA/REPERFUSION INJURY;
D O I
10.3892/ijmm.2016.2544
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
Apelin, the endogenous ligand of APJ which is a member of G protein-coupled receptors, has been shown to be expressed in a variety of tissues in vivo and to exert significant biological effects. Studies have indicated that the apelin/APJ system is involved in the regulation of a variety of physiological functions and pathological processes, and that it is associated with cardiovascular diseases (such as atherosclerosis, hypertension, heart failure and myocardial injury), diabetes with microvascular complications, ischemia reperfusion injury, tumors, pre-eclampsia, as well as others. The occurrence of these diseases is closely related to endothelial dysfunction and the local inflammatory response; however, the occurrence of oxidative stress is related to vascular injury, due to the excessive generation of reactive oxygen species (ROS) and can lead to vascular damage and a series of inflammatory reactions. Therefore, this review summarizes the association between apelin/APJ, oxidative stress and inflammation-related diseases. In addition, drugs targeting the apelin/APJ system are recommended, thus providing a novel therapeutic strategy for oxidative stress-related inflammatory diseases.
引用
收藏
页码:1159 / 1169
页数:11
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