ReviewActa diabetologica2025
The interactions between melatonin and the renin-angiotensin system (RAS) in vascular attenuation in diabetic and non-diabetic conditions.
Review in Acta diabetologica, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
2 citing papers in PubMed.
- Melatonin: Roles and Molecular Mechanisms in Metabolic Dysfunction-Associated Steatotic Liver Disease.Biomolecules · 2026Review
- Histological effect of melatonin and its agonist on testes in light-exposure and pinealectomized rats.Anatomical science international · 2026Article
Corrections and comments
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Authors and funding
3 authors.
Funding
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Abstract
backgroundThe 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 (MT
objectiveThis 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.
conclusionThis 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
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