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Aging and vascular dysfunction: beneficial melatonin effects.

Luigi Fabrizio Rodella¹, Gaia Favero, Claudia Rossini

¹Department of Biomedical Sciences and Biotechnologies, Section of Human Anatomy, University of Brescia, Viale Europa 11, Brescia, Italy.

Age (Dordrecht, Netherlands)

|November 24, 2011

Summary

This summary is machine-generated.

Melatonin, a molecule that activates Sirtuin1 (SIRT1), combats aging-related vascular dysfunction in mice. Extended-release melatonin improved vessel health by modulating SIRT1, p53, and endothelial nitric oxide synthase (eNOS) pathways.

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Area of Science:

Gerontology
Vascular Biology
Molecular Biology

Background:

Aging involves progressive physiological deterioration and cellular loss, impacting vital organs and functions.
Sirtuin1 (SIRT1) is implicated in lifespan extension, but its precise role in aging remains unclear.
Melatonin, a pleiotropic molecule, activates SIRT1 and modulates oxidative stress-induced senescence and pro-survival pathways.

Purpose of the Study:

To evaluate the anti-aging effects of melatonin on vascular health in apolipoprotein E (APOE)-deficient mice.
To investigate the impact of melatonin on SIRT1, p53, endothelial nitric oxide synthase (eNOS), and endothelin-1 (ET-1) markers in aging vessels.

Main Methods:

Apolipoprotein E (APOE)-deficient mice at 6 and 15 weeks were treated with two melatonin formulations (FAST and RETARD).
Morphological changes in the aortic arch were assessed, along with the expression of SIRT1, p53, eNOS, and ET-1.
Comparative analysis of rapid-release (FAST) versus extended-release (RETARD) melatonin efficacy was performed.

Main Results:

SIRT1 and eNOS levels decreased, while p53 and ET-1 expression increased in APOE mice with age (6 to 15 weeks).
Melatonin treatment improved endothelial damage, reduced SIRT1 and eNOS loss, and decreased p53 and ET-1 expression.
The RETARD melatonin formulation demonstrated superior improvement in vessel cytoarchitecture compared to FAST.

Conclusions:

The SIRT1-p53-eNOS axis is a key indicator of age-related vascular dysfunction.
Melatonin effectively counteracts aging-induced vascular impairments in APOE-deficient mice.
Extended-release melatonin (RETARD) is a more effective therapeutic option for mitigating age-related vascular dysfunction.