Melatonin and cardiac pathophysiology

Russel J Reiter, Dun X. Tan

Research output: Contribution to journalArticle

12 Citations (Scopus)

Abstract

Melatonin, an indole produced in several organs but most notably in the pineal gland, has a variety of effects that influence cardiac pathophysiology. Herein, we summarize the findings that illustrate the ability of melatonin to attenuate the severity of hypertension, limit myocardial damage, improve the function of the ischemic-reperfused heart, protect the heart from the toxicity of anthracycline drugs and from an immunosuppressant drug (cyclosporine A), and reduce cardiac hypertrophy and the associated pathophysiology caused by hyperthyroidism. The protective actions of melatonin at the level of the heart probably involve membrane melatonin receptors that exist on cardiomyocytes, in addition functions of melatonin as an antioxidant that are not receptor mediated. Whereas studies to date have been performed primarily in experimental animals, the uncommonly low toxicity of melatonin warrants tests of its utility in humans in cases of cardiac pathophysiology.

Original languageEnglish (US)
Pages (from-to)31-34
Number of pages4
JournalHeart and Metabolism
Issue number44
StatePublished - 2009

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Melatonin
Melatonin Receptors
Pineal Gland
Anthracyclines
Cardiomegaly
Hyperthyroidism
Immunosuppressive Agents
Drug-Related Side Effects and Adverse Reactions
Cardiac Myocytes
Cyclosporine
Antioxidants
Hypertension
Membranes
Pharmaceutical Preparations

Keywords

  • Cardiac hypertrophy
  • Drug toxicity
  • Heart
  • Hypertension
  • Ischemia-reperfusion injury
  • Melatonin

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine
  • Endocrinology, Diabetes and Metabolism

Cite this

Melatonin and cardiac pathophysiology. / Reiter, Russel J; Tan, Dun X.

In: Heart and Metabolism, No. 44, 2009, p. 31-34.

Research output: Contribution to journalArticle

Reiter, Russel J ; Tan, Dun X. / Melatonin and cardiac pathophysiology. In: Heart and Metabolism. 2009 ; No. 44. pp. 31-34.
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