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MINI REVIEW article

Front. Med.
Sec. Geriatric Medicine
Volume 11 - 2024 | doi: 10.3389/fmed.2024.1487971

Melatonin Stabilizes Atherosclerotic Plaques: An Association That Should Be Clinically Exploited

Provisionally accepted
Russel J Reiter Russel J Reiter 1*Ramaswamy Sharma Ramaswamy Sharma 2*Alejandro Romero Alejandro Romero 3Fedor Simko Fedor Simko 4Alberto Dominguez-Rodriguez Alberto Dominguez-Rodriguez 5Daniel P Cardinali Daniel P Cardinali 6,7
  • 1 The University of Texas Health Science Center at San Antonio, San Antonio, Texas, United States
  • 2 University of the Incarnate Word, San Antonio, United States
  • 3 Complutense University of Madrid, Madrid, Madrid, Spain
  • 4 Comenius University, Bratislava, Bratislava, Slovakia
  • 5 Servicio de Cardiología, Hospital Universitario de Canarias, Tenerife, Spain
  • 6 University of Buenos Aires, Buenos Aires, Buenos Aires, Argentina
  • 7 Pontifical Catholic University of Argentina, Buenos Aires, Buenos Aires, Argentina

The final, formatted version of the article will be published soon.

    Atherosclerosis is the underlying factor in the premature death of millions of humans annually. The cause of death is often a result of the rupture of an atherosclerotic plaque followed by discharge of the associated molecular debris into the vessel lumen which occludes the artery leading to ischemia of downstream tissue and to morbidity or mortality of the individual. This is most serious when it occurs in the heart (heart attack) or brain (stroke). Atherosclerotic plaques are classified as either soft, rupture-prone, or hard, rupture resistant. Melatonin, the production of which diminishes with age, has major actions in converting soft to hard plaques. Experimentally, melatonin reduces the ingrowth of capillaries from the tunica media into the plaque relieving pressure on the plaque, reducing intraplaque hemorrhage and limiting the size of the necrotic core. Moreover, melatonin promotes the formation of collagen by invading vascular smooth muscle cells which strengthen the plaque crown making it resistant to rupture. Melatonin is also a powerful antioxidant and anti-inflammatory agent such that is reduces oxidative damage to tissues associated with the plaque and limits inflammation both of which contribute to plaque cap weakness. Additional benefits of melatonin relative to atherosclerosis is inhibition of adhesion molecules on the endothelial cell surface, limiting the invasion of monocytes into the arterial intima, and reducing the conversion of anti-inflammatory M2 macrophages to pro-inflammatory M1 macrophages. Given the high physiological and financial cost of cardiac and neural ischemic events, this information should be given high priority in the clinical setting.

    Keywords: Atherosclerotic plaque, intraplaque hemorrhage, Plaque rupture, Soft plaque, hard plaque, Macrophage polarization, Inflammation, Adhesion molecules, Heart Attack

    Received: 29 Aug 2024; Accepted: 29 Nov 2024.

    Copyright: © 2024 Reiter, Sharma, Romero, Simko, Dominguez-Rodriguez and Cardinali. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

    * Correspondence:
    Russel J Reiter, The University of Texas Health Science Center at San Antonio, San Antonio, 78229, Texas, United States
    Ramaswamy Sharma, University of the Incarnate Word, San Antonio, United States

    Disclaimer: All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers. Any product that may be evaluated in this article or claim that may be made by its manufacturer is not guaranteed or endorsed by the publisher.