Melatonin ameliorates myocardial infarction in obese diabetic individuals: the possible involvement of macrophage apoptotic factors.

In recent days, the hike in obesity mediated epidemic across the globe and prevalence of obesity induced cardiovascular disease (CVD) has become one of the chief grounds of morbidity and mortality. This epidemic driven detrimental events in the cardiac tissues starts with the altered distribution and metabolism pattern of high-density lipoprotein (HDL) and low-density lipoprotein (LDL) leading to cholesterol (oxidized LDL) deposition on arterial wall and atherosclerotic plaque generation, followed by vascular spasm and infarction. Subsequently, obesity triggered metabolic malfunction induce free radical generation which may further trigger pro-inflammatory signalling and nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) transcriptional factor, thus inducing interferon-gamma (IFN-γ), tumour necrosis factor-alpha (TNF-α), and inducible nitric oxide synthase (iNOS). This terrifying cardiomyopathy can be further aggravated in type 2 diabetes mellitus, thereby turning the obese diabetic patients prone towards the development of myocardial infarction or stroke in comparison to their non diabetic counterparts. The accelerated oxidative stress and pro-inflammatory response induced cardiomyocyte hypertrophy, followed by apoptosis in obese diabetic individuals causes progression of athero-thrombotic vascular disease. Being an efficient antioxidative and anti-inflammatory indolamine, melatonin effectively inhibits lipid peroxidation (LPO), pro-inflammatory reactions, thereby resolving free radical induced myocardial damages along with maintaining antioxidant reservoir to preserve cardiovascular integrity. Prolonged melatonin treatment maintains balanced body weight and serum total cholesterol (TC) concentration by inhibiting cholesterol synthesis and promoting cholesterol catabolism. Additionally, melatonin promotes macrophage polarization toward the anti-inflammatory state, providing a proper shield during the recovery period. Therefore, the protective role of melatonin in maintaining the lipid metabolism homeostasis and blocking the atherosclerotic plaque rupture could be targeted as the possible therapeutic strategy for the management of obesity induced acute myocardial infarction (AMI). This review aimed at orchestrating the efficacy of melatonin in ameliorating irrevocable oxidative cardiovascular damage induced by the obesity- diabetes correlation. This article is protected by copyright. All rights reserved.