Melatonin as a protective agent in cardiac ischemia-reperfusion injury: Vision/Illusion?
| Autor: | Puneet Kaur Randhawa, Manish K. Gupta |
|---|---|
| Rok vydání: | 2020 |
| Předmět: |
0301 basic medicine
Receptors Melatonin Myocardial Reperfusion Injury Antioxidants Article Nitric oxide Proinflammatory cytokine Melatonin 03 medical and health sciences chemistry.chemical_compound 0302 clinical medicine medicine Animals Humans Receptor Pharmacology Autophagy Free Radical Scavengers medicine.disease Cell biology 030104 developmental biology chemistry Mitochondrial permeability transition pore Signal transduction Reperfusion injury 030217 neurology & neurosurgery medicine.drug Signal Transduction |
| Zdroj: | Eur J Pharmacol |
| ISSN: | 1879-0712 |
| Popis: | 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. |
| Databáze: | OpenAIRE |
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