The data described in this chapter consider some new information about the benefits of vitamin D3 comparing the results obtained by the authors on the effects of vitamin D3 during oxidative stress with other works available in the literature. In particular, vitamin D3 can induce a concentration-dependent increase in endothelial NO production through eNOS activation consequential to the phosphorylation of p38, AKT, and ERK. Additional information obtained by the author is about the ability of vitamin D3 to prevent the endothelial cell death through modulation of interplay between apoptosis and autophagy. This effect is obtained by inhibiting superoxide anion generation, maintaining mitochondria function and cell viability, activating survival kinases (ERK and Akt), and inducing NO production. The results also describe that vitamin D3 causes human endothelial cell proliferation and migration in a 3-D matrix through NO-dependent mechanisms. These findings support the role of vitamin D3 in the human angiogenic process, suggesting new applications for vitamin D3 in tissue repair and wound healing. Finally, that the authors have demonstrated the ability of vitamin D3 to counteract negative effects of oxidative stress in brain cells. These data suggest the potential therapeutic use of vitamin D to treat or prevent degenerative brain diseases.
Part of the book: A Critical Evaluation of Vitamin D