Abstract

Purpose of reviewMelatonin is a neuroendocrine hormone synthesized primarily by the pineal gland. Numerous studies have suggested that melatonin plays an important role in various cardiovascular diseases. In this article, recent progress regarding melatonin's effects on cardiovascular diseases is reviewed.Recent findingsIn the past year, studies have focused on the mechanism of protection of melatonin on cardiovascular diseases, including myocardial ischemia-reperfusion injury, myocardial hypoxia-reoxygenation injury, pulmonary hypertension, hypertension, atherosclerosis, valvular heart diseases, and other cardiovascular diseases.SummaryStudies have demonstrated that melatonin has significant effects on ischemia-reperfusion injury, myocardial chronic intermittent hypoxia injury, pulmonary hypertension, hypertension, valvular heart diseases, vascular diseases, and lipid metabolism. As an inexpensive and well tolerated drug, melatonin may be a new therapeutic option for cardiovascular disease.

Highlights

  • Melatonin (N-acetyl-5-methoxytryptamine) is a neuroendocrine hormone, which is synthesized primarily by the pineal gland [1]

  • Recent research suggests that melatonin plays an important role in various cardiovascular diseases, including myocardial ischemia-reperfusion injury [7,8], atherosclerosis [9,10], hypertension [11,12], heart failure [13,14], and drug-induced myocardial injury [15,16]

  • Studies have demonstrated that melatonin has significant effects on ischemia-reperfusion injury and myocardial chronic intermittent hypoxia (CIH) injury

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Summary

INTRODUCTION

Melatonin (N-acetyl-5-methoxytryptamine) is a neuroendocrine hormone, which is synthesized primarily by the pineal gland [1]. Several studies have focused on the mechanism of the protection of melatonin on cardiovascular diseases. The aDepartment of Endocrinology and Metabolism, Shanghai Tenth People’s Hospital, School of Medicine, Tongji University, Shanghai, China and bDepartment of Pathology, Division of Neuropathology, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania; Department of Neurology, Weill Cornell Medical College, New York, USA. The work cannot be changed in any way or used commercially

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