Division of Metabolic and Cardiovascular Sciences, Burnett School of Biomedical Sciences, College of Medicine, University of Central Florida, Orlando, FL, 32827, USA.
Division of Metabolic and Cardiovascular Sciences, Burnett School of Biomedical Sciences, College of Medicine, University of Central Florida, Orlando, FL, 32827, USA.
Eur J Pharmacol. 2020 Oct 15;885:173506. doi: 10.1016/j.ejphar.2020.173506. Epub 2020 Aug 26.
Melatonin, an emphatic endogenous molecule exerts protective effects either via activation of G-protein coupled receptors (Melatonin receptors, MTR 1-3), tumor necrosis factor receptor (TNFR), toll like receptors (TLRS), nuclear receptors (NRS) or by directly scavenging the free radicals. MTRs are extensively expressed in the heart as well as in the coronary vasculature. Accumulating evidences have indicated the existence of a strong correlation between reduction in the circulating level of melatonin and precipitation of heart attack. Apparently, melatonin exhibits cardioprotective effects via modulating inextricably interlinked pathways including modulation of mitochondrial metabolism, mitochondrial permeability transition pore formation, nitric oxide release, autophagy, generation of inflammatory cytokines, regulation of calcium transporters, reactive oxygen species, glycosaminoglycans, collagen accumulation, and regulation of apoptosis. Convincingly, this review shall describe the various signaling pathways involved in salvaging the heart against ischemia-reperfusion injury.
褪黑素是一种有力的内源性分子，通过激活 G 蛋白偶联受体（褪黑素受体 1-3，MTR1-3）、肿瘤坏死因子受体（TNFR）、 Toll 样受体（TLRS）、核受体（NRS），或直接清除自由基来发挥保护作用。MTR 在心脏以及冠状动脉血管中广泛表达。越来越多的证据表明，循环褪黑素水平降低与心脏病发作之间存在很强的相关性。显然，褪黑素通过调节相互关联的途径来发挥心脏保护作用，包括调节线粒体代谢、线粒体通透性转换孔形成、一氧化氮释放、自噬、炎症细胞因子生成、钙转运体调节、活性氧、糖胺聚糖、胶原蛋白积累和细胞凋亡调节。令人信服的是，本综述将描述挽救心脏免受缺血再灌注损伤的各种信号通路。
