Abstract
The active metabolites of vitamin D3 (D3) and lumisterol (L3) exert a variety of antiaging and photoprotective effects on the skin. These are achieved through immunomodulation and include anti-inflammatory actions, regulation of keratinocytes proliferation, and differentiation programs to build the epidermal barrier necessary for maintaining skin homeostasis. In addition, they induce antioxidative responses, inhibit DNA damage and induce DNA repair mechanisms to attenuate premature skin aging and cancerogenesis. The mechanism of action would involve interaction with multiple nuclear receptors including VDR, AhR, LXR, reverse agonism on RORα and -γ, and nongenomic actions through 1,25D3-MARRS receptor and interaction with the nongenomic binding site of the VDR. Therefore, active forms of vitamin D3 including its canonical (1,25(OH)2D3) and noncanonical (CYP11A1-intitated) D3 derivatives as well as L3 derivatives are promising agents for the prevention, attenuation, or treatment of premature skin aging. They could be administrated orally and/or topically. Other forms of parenteral application of vitamin D3 precursor should be considered to avoid its predominant metabolism to 25(OH)D3 that is not recognized by CYP11A1 enzyme. The efficacy of topically applied vitamin D3 and L3 derivatives needs further clinical evaluation in future trials.
Highlights
Skin, like any other organs, undergoes progressive decline in its physiological, morphological, and functional features during aging [1,2,3,4]
Air pollutants, persistent organic pollutants, and heavy metals can behave like endocrine-disrupting chemicals (EDCs), which may cause vitamin D deficiency directly or indirectly
In the alternative pathway, vitamin D3 can be activated by CYP11A1 with further modification by other cytochrome enzymes leading to production of large number of metabolites in humans [21,36,138,139,140,141,142] (Figure 1), some of which are non- or low-calcemic at high, therapeutic, doses [143,144,145,146]
Summary
Like any other organs, undergoes progressive decline in its physiological, morphological, and functional features during aging [1,2,3,4]. Air pollutants, persistent organic pollutants, and heavy metals can behave like endocrine-disrupting chemicals (EDCs), which may cause vitamin D deficiency directly or indirectly. The latter would be secondary to a weight gain, the dysregulation of parathyroid hormone and calcium homeostasis, and a thyroid dysfunction [57,58]. The capacity of the skin to produce vitamin D3 decreases (irrespective of the season), and the degradation of its active forms increases [59,60]. We aimed to discuss the significance of vitamin D in the skin aging process
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