Inhibition of platelet activation using vitamins

Kobzar, Gennadi

doi:10.1080/09537104.2019.1652262

Cited by 7 publications

(10 citation statements)

References 90 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…A potential explanation for the protective effect of vitamin C on CES is that vitamin C might be associated with a decreased risk of atrial fibrillation, a well-known leading cause of CES [36,37]. It has also been reported that vitamin C exhibits antiplatelet properties by inhibiting the formation of thromboxane A2 and stimulating the synthesis of prostaglandin E1 [38]. Despite such biologically plausible explanations, further studies are warranted to determine the exact underlying mechanisms.…”

Section: Vitamin C and Strokementioning

confidence: 99%

The impact of plasma vitamin C levels on the risk of cardiovascular diseases and Alzheimer's disease: A Mendelian randomization study

et al. 2021

View full text Add to dashboard Cite

Background & aims: Previous observational studies have reported associations between plasma vitamin C levels, and cardiovascular diseases (CVDs) and Alzheimer's disease (AD); however, no conclusive results have been obtained. We conducted a Mendelian randomization (MR) study to investigate the causality of vitamin C on the risk of nine CVDs [including coronary artery disease (CAD), myocardial infarction (MI), atrial fibrillation (AF), heart failure (HF), stroke, ischemic stroke (IS), and IS subtypes] and Alzheimer's disease. Methods: Eleven single-nucleotide polymorphisms (SNPs) identified in a recent genome-wide metaanalysis (N ¼ 52,018) were used as the instrumental variables for plasma vitamin C levels. The summarylevel data for CVDs and AD were extracted from consortia and genome-wide association studies (GWAS). We performed MR analyses using the fixed-effects inverse-variance-weighted (IVW) method, weighted median, and MR-Egger approaches.Results: This MR study found suggestive evidence that genetic liability to higher vitamin C levels was associated with a lower risk of cardioembolic stroke [odds ratio (OR, presented per 1 standard deviation increase in plasma vitamin C levels) ¼ 0.773; 95% confidence interval (CI), 0.623e0.959; P ¼ 0.020] and AD (OR ¼ 0.968; 95% CI, 0.946e0.991; P ¼ 0.007) using the fixed-effects IVW method. Sensitivity analysis yielded directionally similar results. A null-association was observed between vitamin C and the other CVDs. Conclusion: Our MR study provided suggestive evidence that higher vitamin C levels were casually associated with a decreased risk of cardioembolic stroke and AD. No evidence was observed to suggest that vitamin C affected the risk of CAD, MI, AF, HF, stroke, IS, large artery stroke, or small vessel stroke. However, well-designed studies are warranted to confirm these results and determine the underlying mechanisms of the causal links.

show abstract

Section: Vitamin C and Strokementioning

confidence: 99%

The impact of plasma vitamin C levels on the risk of cardiovascular diseases and Alzheimer's disease: A Mendelian randomization study

et al. 2021

View full text Add to dashboard Cite

show abstract

“…Extensively reviewed by Kobzar et al, some vitamins, including vitamin A, D, B 6 and C, can act as inhibitors of platelet activation by inhibiting biochemical pathways or preventing damage to vessel walls [134]. Particularly in combination, vitamins may act synergistically to enhance the effects of endogenous anti-platelet compounds, such as prostacyclin or nitric oxide [134]. The vitamins with the most potent antiplatelet activity are vitamins A and D [134].…”

Section: Vitamins and Polyphenolsmentioning

confidence: 99%

“…Particularly in combination, vitamins may act synergistically to enhance the effects of endogenous anti-platelet compounds, such as prostacyclin or nitric oxide [134]. The vitamins with the most potent antiplatelet activity are vitamins A and D [134]. Specifically, vitamin A inhibits intracellular calcium release and platelet inhibition via the binding of an intracellular retinoid X receptor with a G-coupled protein [134,135], and vitamin D inhibits platelet aggregation by modulating endothelial cells [134].…”

Section: Vitamins and Polyphenolsmentioning

confidence: 99%

“…The vitamins with the most potent antiplatelet activity are vitamins A and D [134]. Specifically, vitamin A inhibits intracellular calcium release and platelet inhibition via the binding of an intracellular retinoid X receptor with a G-coupled protein [134,135], and vitamin D inhibits platelet aggregation by modulating endothelial cells [134]. Fruits are a source of vitamins and moreover polyphenols, which together may induce antioxidant effects and reduce platelet activation [136].…”

Section: Vitamins and Polyphenolsmentioning

confidence: 99%

“…For instance, high concentrations of phenolic compounds can be found in fresh berries and berry extracts, i.e., phenolic acid and flavonoids [136]. Specifically in combination, vitamins and polyphenols can inhibit platelet activation via antioxidant effects, modulation of endothelial cells or inhibiting intracellular calcium release [134,136].…”

Section: Vitamins and Polyphenolsmentioning

confidence: 99%

See 2 more Smart Citations

Effects of Nutrients on Platelet Function: A Modifiable Link between Metabolic Syndrome and Neurodegeneration?

Arnoldussen

Witkamp

2021

Biomolecules

View full text Add to dashboard Cite

Metabolic syndrome increases the risk of vascular dementia and other neurodegenerative disorders. Recent studies underline that platelets play an important role in linking peripheral with central metabolic and inflammatory mechanisms. In this narrative review, we address the activation of platelets in metabolic syndrome, their effects on neuronal processes and the role of the mediators (e.g., serotonin, platelet-derived growth factor). Emerging evidence shows that nutritional compounds and their metabolites modulate these interactions—specifically, long chain fatty acids, endocannabinoids and phenolic compounds. We reviewed the role of activated platelets in neurovascular processes and nutritional compounds in platelet activation.

show abstract

Reeling in complement in transplant‐associated thrombotic microangiopathy: You're going to need a bigger boat

Jodele

Sabulski

2023

American J Hematol

View full text Add to dashboard Cite

Over the last decade there have been numerous advances in both the diagnosis and treatment of transplant-associated thrombotic microangiopathy (TA-TMA). These are largely the result of an improved understanding of complement activation in TA-TMA and the ability to prevent end organ injury and death with timely initiation of complementblocking therapies. In this article, we review our current understanding of the pathophysiology of TA-TMA, particularly as it pertains to complement activation, endothelial injury, and clinical management. We then review novel complement-blocking therapies that are currently under investigation for use in TA-TMA, as well as discuss special considerations for complement-blocking therapy in hematopoietic stem cell transplant recipients. Through these reviews we aim to answer or at least provide an educated discussion on the most commonly posed TA-TMA management questions and dilemmas.

show abstract

Inhibition of platelet activation using vitamins

Cited by 7 publications

References 90 publications

The impact of plasma vitamin C levels on the risk of cardiovascular diseases and Alzheimer's disease: A Mendelian randomization study

The impact of plasma vitamin C levels on the risk of cardiovascular diseases and Alzheimer's disease: A Mendelian randomization study

Effects of Nutrients on Platelet Function: A Modifiable Link between Metabolic Syndrome and Neurodegeneration?

Reeling in complement in transplant‐associated thrombotic microangiopathy: You're going to need a bigger boat

Contact Info

Product

Resources

About