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GLP-1(28-36a) 的心脏保护作用:降解产物还是 GLP-1 的更佳搭档?

Cardioprotective effects of GLP-1(28-36a): A degraded metabolite or GLP-1's better half?

机构信息

Department of Diabetes and Endocrinology, Gifu University Graduate School of Medicine, Gifu, Japan.

Yutaka Seino Distinguished Center for Diabetes Research, Kansai Electric Power Medical Research Institute, Kobe, Japan.

出版信息

J Diabetes Investig. 2020 Nov;11(6):1422-1425. doi: 10.1111/jdi.13302. Epub 2020 Jun 24.

Abstract

Molecular mechanism underlying glucagon-like peptide-1 exertion of cardioprotective effects in glucagon-like peptide-1 receptor-dependent and -independent manners. Glucagon-like peptide-1 (28-36a) enters coronary artery endothelial cells through macropinocytosis and binds to mitochondrial trifunctional protein-α, shifting substrate utilization to increase adenosine triphosphate production and modulating a adenosine triphosphate-sensor soluble adenylyl cyclase, thereby producing cyclic adenosine monophosphate and activating protein kinase A to exert cytoprotection from oxidative injury.

摘要

胰高血糖素样肽-1 发挥其心脏保护作用的分子机制:依赖于胰高血糖素样肽-1 受体和不依赖于胰高血糖素样肽-1 受体的方式。胰高血糖素样肽-1(28-36a)通过巨胞饮作用进入冠状动脉内皮细胞,并与线粒体三功能蛋白-α结合,改变底物利用以增加三磷酸腺苷的产生,并调节三磷酸腺苷传感器可溶性腺苷酸环化酶,从而产生环磷酸腺苷并激活蛋白激酶 A,发挥抗氧化损伤的细胞保护作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/10d9/7610112/0b01e47e144d/JDI-11-1422-g001.jpg

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