International Journal of Molecular Sciences · 5 authors, 3 centres
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This narrative review examines the molecular mechanisms by which vitamin D counteracts aging processes such as immunosenescence and inflammaging. A key limitation is the lack of clear cause-effect relationships and the need for more clinical research to translate findings into practice.
Aging involves immunosenescence and inflammaging, contributing to chronic diseases and reduced quality of life. Vitamin D, a micronutrient with immunomodulatory properties, may counteract these processes. Methods: This is a narrative review synthesizing literature on cellular and molecular mechanisms, including in vitro and in vivo studies on immune cells, cardiomyocytes, and skeletal muscle cells. Key Results: Vitamin D regulates immune responses by inhibiting pro-inflammatory cytokines (e.g., TNF-α, IL-6), enhancing anti-inflammatory cytokines (e.g., IL-10), and targeting NF-kB signaling to reduce inflammation. It delays cellular senescence, improves mitochondrial function, and protects against oxidative stress. In heart and skeletal muscle, vitamin D counteracts age-related dysfunction by inhibiting NF-kB and reducing sarcopenia. Limitations: The review highlights that cause-effect relationships are not always established, animal studies may not be translatable to humans, and there is variability in vitamin D assessment and supplementation guidelines. Implications: Vitamin D supplementation may support healthy aging, but further clinical research is needed to establish optimal dosages and clinical applications, especially in elderly populations.
