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Background <p>The hormone melatonin (MEL), primarily acknowledged for its role in regulating circadian rhythms, has demonstrated itself to be a complicated molecule with significant implications for vascular physiology. Melatonin exerts extensive physiological effects directly <i>via</i> the MEL receptor type 1 (MT<sub>1</sub>R) and the MEL receptor type 2 (MT<sub>2</sub>R), as well as indirectly through the improvement of antioxidant vascular tone.</p> Objective <p>This review aims to analyse the intricate relationships between MEL and the renin–angiotensin system (RAS) in the vascular attenuation of non-diabetic (non-DM) and diabetic (DM) contexts. Alterations in the expression of RAS components and their dysregulation are prevalent in diabetes. Melatonin exhibits vasoprotective advantages in non-diabetic conditions. In the context of DM, vascular problrms such as vascular endothelial dysfunction (VED), hypertension, and atherosclerosis result from the dysregulation of MEL-RAS interactions. Comprehending the actions of MEL on RAS components in diabetes vasculature is essential for formulating tailored pharmaceutical therapy methods.</p> Conclusion <p>This review consolidates existing knowledge regarding the vascular effects of MEL in relation to RAS activation, emphasising its potential role as a modulating factor for angiotensin 1–8 (Ang 1–8), angiotensin-converting enzyme 2 (ACE<sub>2</sub>), and angiotensin 1–7 (Ang 1–7) in the management of vascular complications associated with DM.</p>

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The interactions between melatonin and the renin–angiotensin system (RAS) in vascular attenuation in diabetic and non-diabetic conditions

  • 期刊论文

  • 发表日期：

    2025年3月13日

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  • Nazar M. Shareef Mahmood,
  • Almas M. R. Mahmud,
  • Ismail M. Maulood

摘要

Background

The hormone melatonin (MEL), primarily acknowledged for its role in regulating circadian rhythms, has demonstrated itself to be a complicated molecule with significant implications for vascular physiology. Melatonin exerts extensive physiological effects directly via the MEL receptor type 1 (MT1R) and the MEL receptor type 2 (MT2R), as well as indirectly through the improvement of antioxidant vascular tone.

Objective

This review aims to analyse the intricate relationships between MEL and the renin–angiotensin system (RAS) in the vascular attenuation of non-diabetic (non-DM) and diabetic (DM) contexts. Alterations in the expression of RAS components and their dysregulation are prevalent in diabetes. Melatonin exhibits vasoprotective advantages in non-diabetic conditions. In the context of DM, vascular problrms such as vascular endothelial dysfunction (VED), hypertension, and atherosclerosis result from the dysregulation of MEL-RAS interactions. Comprehending the actions of MEL on RAS components in diabetes vasculature is essential for formulating tailored pharmaceutical therapy methods.

Conclusion

This review consolidates existing knowledge regarding the vascular effects of MEL in relation to RAS activation, emphasising its potential role as a modulating factor for angiotensin 1–8 (Ang 1–8), angiotensin-converting enzyme 2 (ACE2), and angiotensin 1–7 (Ang 1–7) in the management of vascular complications associated with DM.