Dose rectification of an imbalance between DPP4 and GLP-1 ameliorates chronic stress-related vascular aging and atherosclerosis?

被引:7
作者
Cheng, Xian Wu [1 ,2 ,3 ]
Narisawa, Megumi [4 ]
Jin, Enze [5 ]
Yu, Chenglin [1 ]
Xu, Wenhu [1 ]
Piao, Limei [1 ]
机构
[1] Yanbian Univ Hosp, Dept Cardiol, Yanji, Jilin, Peoples R China
[2] Kyung Hee Univ, Dept Internal Med, Div Cardiol, Seoul, South Korea
[3] Nagoya Univ, Inst Innovat Future Soc, Grad Sch Med, Nagoya, Aichi, Japan
[4] Tajimikenlitsu Gen Hosp, Dept Cardiol, Tajimi, Gifu, Japan
[5] Harbin Med Univ, Dept Cardiol, Hosp 4, Harbin, Heilongjiang, Peoples R China
来源
CLINICAL AND EXPERIMENTAL PHARMACOLOGY AND PHYSIOLOGY | 2018年 / 45卷 / 05期
关键词
atherosclerosis; chronic stress; dipeptidyl peptidase-4; inflammation; vascular senescence; CYSTEINE PROTEASE CATHEPSINS; CORONARY-HEART-DISEASE; CARDIOVASCULAR-DISEASE; MYOCARDIAL-INFARCTION; PROTHROMBOTIC STATE; INSULIN-RESISTANCE; MURINE MODEL; RISK; EXENATIDE; NEOVASCULARIZATION;
D O I
10.1111/1440-1681.12903
中图分类号
R9 [药学];
学科分类号
1007 ;
摘要
Exposure to psychosocial stress is a risk factor for cardiovascular disease, including vascular aging and regeneration. Dipeptidyl peptidase-4 (DPP-4) exerts many physiological and pharmacological functions by regulating its extremely abundant substrates [eg., glucagon-like peptide-1 (GLP-1), stromal cell-derived factor-1/C-X-C chemokine receptor type-4, etc.]. Over the past decade, emerging data has revealed unexpected roles for DPP-4 and GLP-1 in intracellular signaling, oxidative stress production, lipid metabolism, cell apoptosis, immune activation, insulin resistance, and inflammation. This mini review focuses on recent findings in this field, highlighting an imbalance between DPP4 and GLP-1 as a potential therapeutic target in the management of vascular aging and atherosclerosis in animals under experimental stress conditions.
引用
收藏
页码:467 / 470
页数:4
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