Abstract
Melatonin is a pleiotropic, indole secreted, and synthesized by the human pineal gland. Melatonin has biological effects including anti-apoptosis, protecting mitochondria, anti-oxidation, anti-inflammation, and stimulating target cells to secrete cytokines. Its protective effect on cardiomyocytes in acute myocardial infarction (AMI) has caused widespread interest in the actions of this molecule. The effects of melatonin against oxidative stress, promoting autophagic repair of cells, regulating immune and inflammatory responses, enhancing mitochondrial function, and relieving endoplasmic reticulum stress, play crucial roles in protecting cardiomyocytes from infarction. Mitochondrial apoptosis and dysfunction are common occurrence in cardiomyocyte injury after myocardial infarction. This review focuses on the targets of melatonin in protecting cardiomyocytes in AMI, the main molecular signaling pathways that melatonin influences in its endogenous protective role in myocardial infarction, and the developmental prospect of melatonin in myocardial infarction treatment.
Highlights
With the general improvement of the human living standard, the change of living habits and the prolongation of life span, the prevalence rate of cardiovascular diseases has risen sharply
Cytokine release and the inflammatory response are important conditions for tissue healing after myocardial infarction, but an excessive inflammatory response leads to myocardial tissue remodeling, activating apoptosis signals in cardiomyocytes with destruction of the integrity of extracellular matrix, which is not conducive to the survival of cardiomyocytes and the recovery of cardiac function (Nahrendorf et al, 2010; Krause et al, 2018)
Caspase-8 is involved in fatty acid synthase (Fas)/FasL-related death receptor pathway, caspase-9 is depended on mitochondrial damage, and caspase-12 is related to endoplasmic reticulum stress (Fuhrmann and Brune, 2017; Karwi et al, 2018; Jiang et al, 2019)
Summary
Zhenhong Fu1*†, Yang Jiao1†, Jihang Wang, Ying Zhang, Mingzhi Shen, Russel J. Reviewed by: Ying Tan, Southern Medical University, China Ana Beatriz Rodríguez, University of Extremadura, Spain Jian Yang, Fourth Military Medical University, China. Melatonin has biological effects including anti-apoptosis, protecting mitochondria, anti-oxidation, anti-inflammation, and stimulating target cells to secrete cytokines. Its protective effect on cardiomyocytes in acute myocardial infarction (AMI) has caused widespread interest in the actions of this molecule. The effects of melatonin against oxidative stress, promoting autophagic repair of cells, regulating immune and inflammatory responses, enhancing mitochondrial function, and relieving endoplasmic reticulum stress, play crucial roles in protecting cardiomyocytes from infarction. This review focuses on the targets of melatonin in protecting cardiomyocytes in AMI, the main molecular signaling pathways that melatonin influences in its endogenous protective role in myocardial infarction, and the developmental prospect of melatonin in myocardial infarction treatment
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
