Melatonin as a treatment for atherosclerosis: focus on programmed cell death, inflammation and oxidative stress

Abstract

Delaying the development of atherosclerosis (AS) and decreasing cardiac ischemia-reperfusion damage remain serious challenges for the medical community. Chronic arterial disease, i.e., AS, is frequently linked to oxidative stress and inflammation as significant contributing causes. AS risk factors, such as hyperlipidemia, high blood pressure, age, hyperglycemia, smoking, high cholesterol, and irregular sleep patterns, can exacerbate AS in the carotid artery and further shrink its lumen. Finding new approaches that support plaque inhibition or stability is an ongoing problem. The last ten years have shown us that melatonin (MLT) affects the cardiovascular system, although its exact mechanisms of action are yet unknown. MLT's direct free radical scavenger activity, its indirect antioxidant qualities, and its anti-inflammatory capabilities all contribute to its atheroprotective effects on several pathogenic signaling pathways. Herein, we examine the evidence showing that MLT treatment has significant protective effects against AS and AS-related cardiovascular diseases. The numerous pieces of the puzzle that have been as for epigenetic and biogenetic targets for prevention and therapy against the atherosclerotic pathogenic processes are identified.