Vitamin D Promotes Protein Homeostasis and Longevity via the Stress Response Pathway Genes skn-1, ire-1, and xbp-1
Cell Rep, 17 (5), 1227-1237 2016 Oct 25, DOI: 10.1016/j.celrep.2016.09.086
Mortality category in VitaminDWiki starts with:
People die sooner if they have low vitamin D
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- Life extension and health improvement: Calico (Google) and perhaps Vitamin D
- Contains the following was made by the founder of VitaminDWiki in 2013
- Vitamin D and co-factors will square the curve (live longer AND healthier)
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- Current Perspective in the Discovery of Anti-aging Agents from Natural Products - Oct 2017 FREE PDF
- The Death D-fying Vitamin - June 2018 Dr. Holick, Mayo Clinic FREE PDF
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Karla A Mark 1, Kathleen J Dumas 2, Dipa Bhaumik 1, Birgit Schilling 1, Sonnet Davis 1, Tal Ronnen Oron 1, Dylan J Sorensen 1, Mark Lucanic 1, Rachel B Brem 1, Simon Melov 1, Arvind Ramanathan 1, Bradford W Gibson 1, Gordon J Lithgow 3
Vitamin D has multiple roles, including the regulation of bone and calcium homeostasis. Deficiency of 25-hydroxyvitamin D, the major circulating form of vitamin D, is associated with an increased risk of age-related chronic diseases, including Alzheimer's disease, Parkinson's disease, cognitive impairment, and cancer. In this study, we utilized Caenorhabditis elegans to examine the mechanism by which vitamin D influences aging. We found that vitamin-D3-induced lifespan extension requires the stress response pathway genes skn-1, ire-1, and xbp-1. Vitamin D3 (D3) induced expression of SKN-1 target genes but not canonical targets of XBP-1. D3 suppressed an important molecular pathology of aging, that of widespread protein insolubility, and prevented toxicity caused by human β-amyloid. Our observation that D3 improves protein homeostasis and slows aging highlights the importance of maintaining appropriate vitamin D serum levels and may explain why such a wide variety of human age-related diseases are associated with vitamin D deficiency.
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