There is emerging evidence to suggest that vitamin D deficiency is associated
with adverse outcomes in COVID-19 patients. Conversely, vitamin D supplementation
protects against an initial alveolar diffuse damage of COVID-19 becoming
progressively worse. The mechanisms by which vitamin D deficiency exacerbates
COVID-19 pneumonia remain poorly understood. In this review we describe the
rationale of the putative role of endothelial dysfunction in this event. Herein,
we will briefly review (1) anti-inflammatory and anti-thrombotic effects of
vitamin D, (2) vitamin D receptor and vitamin D receptor ligand, (3) protective
role of vitamin D against endothelial dysfunction, (4) risk of vitamin D
deficiency, (5) vitamin D deficiency in association with endothelial dysfunction,
(6) the characteristics of vitamin D relevant to COVID-19,
(7) the role of vitamin D on innate and adaptive response, (8)
biomarkers of endothelial cell activation contributing to cytokine storm, and (9)
the bidirectional relationship between inflammation and homeostasis. Finally, we
hypothesize that endothelial dysfunction relevant to vitamin D deficiency results
from decreased binding of the vitamin D receptor with its ligand on the vascular
endothelium and that it may be immune-mediated via increased interferon 1