Vitamin D for the prevention of cardiovascular disease: Are we ready for that?

Carvalho, Luiz Sérgio F.; Sposito, Andrei C.

doi:10.1016/j.atherosclerosis.2015.06.034

Cited by 66 publications

(41 citation statements)

References 96 publications

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“…However, the mechanism underlying the role of vitamin D in cardiovascular outcomes remains largely elusive. Increased oxidative stress and impaired vascular endothelial function have been suggested to be partly responsible for the adverse cardiovascular outcomes associated with low vitamin D in both animal and human studies [19]. Vitamin D has been shown to increase activity and expression of endothelial nitric oxide synthase (eNOS), the enzyme critical to the generation and bioavailability of nitric oxide [20, 21].…”

Section: Discussionmentioning

confidence: 99%

Vitamin D supplementation lowers thrombospondin-1 levels and blood pressure in healthy adults

et al. 2017

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IntroductionVitamin D insufficiency, defined as 25-hydroxyvitamin D (25(OH)D) levels < 75nmol/L is associated with cardio-metabolic dysfunction. Vitamin D insufficiency is associated with inflammation and fibrosis, but it remains uncertain whether these anomalies are readily reversible. Therefore, we aimed to determine the effects of vitamin D supplementation on markers of: 1) nitric oxide (NO) signaling, 2) inflammation, and 3) fibrosis, in healthy volunteers with mild hypovitaminosis.MethodsHealthy volunteers (n = 35) (mean age: 45 ± 11 years) with 25(OH)D levels <75nmol/L, received vitamin D supplementation (Ostelin ® capsules 2000IU) for 12 weeks. Resting systolic and diastolic blood pressures (BP) were assessed. Routine biochemistry was examined. Plasma concentrations of asymmetric dimethylarginine (ADMA), thrombospondin-1 (TSP-1), plasminogen activator inhibitor-1 (PAI-1), hs-CRP, activin-A, and follistatin-like 3 (FSTL3) were quantitated.ResultsVitamin D administration for 12 weeks significantly increased 25-(OH)D levels (48.8 ± 16 nmol/L to 100.8 ± 23.7 nmol/L, p<0.001). There was significant lowering of systolic and diastolic BP, while there was no significant change in lipid profiles, or fasting insulin. Plasma concentrations of ADMA, hs-CRP, PAI-1, activin A, and FSTL-3 did not change with vitamin D supplementation. However, there was a marked reduction of TSP-1 (522.7 ± 379.8 ng/mL vs 206.7 ± 204.5 ng/mL, p<0.001).ConclusionsVitamin D supplementation in vitamin D insufficient, but otherwise healthy individuals markedly decreased TSP-1 levels and blood pressure. Since TSP-1 suppresses signaling of NO, it is possible that the fall in BP is engendered by restoration of NO effect.

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Section: Discussionmentioning

confidence: 99%

Vitamin D supplementation lowers thrombospondin-1 levels and blood pressure in healthy adults

et al. 2017

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“…Clinical reports have confirmed that vitamin D could regulate blood pressure in healthy individuals [15] and decrease high blood pressure in patients [15, 16]. Moreover, vitamin D receptors have been found in endothelial cells, which suggests that vitamin D may be a regulator of endothelial cell function by inducing key enzyme expression [9]. Although vitamin D has shown valuable effects on endothelial cell physiology, little is known about the molecular mechanisms by which it mediates endothelial cell protection.…”

Section: Introductionmentioning

confidence: 89%

Vitamin D Ameliorates Angiotensin II-Induced Human Endothelial Progenitor Cell Injury via the PPAR-γ/HO-1 Pathway

et al. 2019

J Vasc Res

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Vitamin D has an important protective effect on chronic inflammatory disease. Angiotensin II (AngII) triggers vascular damage and plays a key role in vascular diseases via several mechanisms, including inflammation. Conversely, vitamin D has been shown to have an important protective effect on chronic inflammation. There is evidence showing that vitamin D can reverse the effects of AngII, but the molecular mechanisms by which this occurs are not known. Our results demonstrate that vitamin D improved the viability, migration ability, and tube formation of AngII-pretreated endothelial progenitor cells (EPCs) and inhibited the apoptosis of EPCs induced by AngII. Vitamin D also reversed reactive oxygen species production, vascular inflammatory cytokine generation, and nuclear factor kappa-B activation in EPCs induced by AngII. Furthermore, EPC pretreatment with GW9662 (the antagonist for PPAR-γ) or siHO-1 decreased the protective effect of vitamin D on AngII-induced EPC injury. Overall, our data indicate that vitamin D ameliorated AngII-induced abnormal EPC injury by decreasing oxidative stress and inflammatory cytokine levels. These findings also suggest that vitamin D protected EPCs from AngII-induced vascular injury via the activation of the PPAR-γ/HO-1 signaling pathway.

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“…Vitamin D has well known effects in endothelial cells, where it stimulates nitric oxide (NO) production [54], protects against oxidative stress [58] and prevent endothelial apoptosis [55, 56] by diverse genomic and non-genomic pathways. As endothelial function has emerged as a key factor for initiation and progression of atherosclerotic process, vitamin D may contribute for reversing atherosclerosis burden [57]. A broad series of in vitro studies have also suggested that vitamin D and its analogs consistently suppress pro-inflammatory cytokines and increases anti-inflammatory cytokines, which mechanisms involved seem to be related to the inhibition of NF-kB and p38 pathways by VDRs [58].…”

Section: Relationship Between 25ohd Deficiency and A Variety Of Chronmentioning

confidence: 99%

Vitamin D and Chronic Diseases

et al. 2017

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Vitamin D is one of the essential nutrients to sustain the human health. As a member of the steroid hormone family, it has a classic role in regulating metabolism of calcium and a non-classic role in affecting cell proliferation and differentiation. Epidemiological studies have shown that 25OHD deficiency is closely associated with common chronic diseases such as bone metabolic disorders, tumors, cardiovascular diseases, and diabetes. 25OHD deficiency is also a risk factor for neuropsychiatric disorders and autoimmune diseases. 25OHD deficiency is highly prevalent in the world. It is therefore necessary to know the adverse health effects of 25OHD deficiency, and to design interventions and early treatments for those who are likely to have low levels of 25OHD.

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Vitamin D for the prevention of cardiovascular disease: Are we ready for that?

Cited by 66 publications

References 96 publications

Vitamin D supplementation lowers thrombospondin-1 levels and blood pressure in healthy adults

Vitamin D supplementation lowers thrombospondin-1 levels and blood pressure in healthy adults

Vitamin D Ameliorates Angiotensin II-Induced Human Endothelial Progenitor Cell Injury via the PPAR-γ/HO-1 Pathway

Vitamin D and Chronic Diseases

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