Abstract
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 α. A possible sequence of events may be described as (1) angiotensin II converting enzyme-related initial endothelial injury followed by vitamin D receptor-related endothelial dysfunction, (2) endothelial lesions deteriorating to endothelialitis, coagulopathy and thrombosis, and (3) vascular damage exacerbating pulmonary pathology and making patients with vitamin D deficiency vulnerable to death.
Highlights
There is emerging evidence to suggest that vitamin D deficiency is associated with an increased risk of acquiring COVID19 infection (Meltzer et al, 2020), as well as developing COVID19-associated thrombosis (Weir et al, 2020)
A review suggests that endothelial dysfunction contributes to COVID-19-assocated vascular inflammation and coagulopathy (Zhang et al, 2020), ; questions remain regarding the role of endothelial dysfunction in COVID-19 patients with vitamin D deficiency
Vitamin D deficiency was shown to be associated with endothelial dysfunction in patients with stable systemic lupus erythematosus (SLE) and that endothelial function improved after 12 weeks of treatment with 1,25(OH)2D3 (Reynolds et al, 2016)
Summary
There is emerging evidence to suggest that vitamin D deficiency is associated with an increased risk of acquiring COVID19 infection (Meltzer et al, 2020), as well as developing COVID19-associated thrombosis (Weir et al, 2020). On the other hand, increasing evidence suggests that vitamin D supplementation prevents COVID19 infection-induced multi-organ damage (Aygun, 2020), coagulopathy (Ali, 2020), and mortality (Grant et al, 2020; Ilie et al, 2020). A review suggests that endothelial dysfunction contributes to COVID-19-assocated vascular inflammation and coagulopathy (Zhang et al, 2020), ; questions remain regarding the role of endothelial dysfunction in COVID-19 patients with vitamin D deficiency. The answers to these questions would provide essential insights into the mechanisms of COVID19 in patients with vitamin D deficiency, and potential therapeutic targets. We hypothesize endothelial dysfunction may play a role in COVID-19 patients with vitamin D deficiency
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