The Vitamin K Cycle

Oldenburg, Johannes; Marinova, Milka; Müller-Reible, Clemens; Watzka, Matthias

doi:10.1016/s0083-6729(07)00003-9

Cited by 153 publications

(116 citation statements)

References 129 publications

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“…10% of all adverse drug reactions leading to hospital admission. 4 Warfarin works by inhibiting the C1 subunit of vitamin K epoxide reductase enzyme (encoded by VKORC1 ) and by interfering with cyclic interconversion of vitamin K 5 essential for the activation of vitamin K-dependent clotting factors such as II, VII, IX, and X as well as endogenous anticoagulant factors, protein C, and protein S. 6 Clinically available warfarin is a racemic molecule, which presents as S -warfarin and R -warfarin. 7 S -warfarin, compared with R -warfarin, is approximately fi ve times more active as a VKOR inhibitor and is converted to inactive metabolites by CYP2C9, encoded by CYP2C9 .…”

Section: [ 1 4 8 # 3 C H E S T S E P T E M B E R 2 0 1 5 ]mentioning

confidence: 99%

Meta-analysis of Randomized Controlled Trials of Genotype-Guided vs Standard Dosing of Warfarin

Dahal

Sharma

Fung

et al. 2015

CHEST

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BACKGROUND:Warfarin is a widely prescribed anticoagulant, and its eff ect depends on various patient factors including genotypes. Randomized controlled trials (RCTs) comparing genotypeguided dosing (GD) of warfarin with standard dosing have shown mixed effi cacy and safety outcomes. We performed a meta-analysis of all published RCTs comparing GD vs standard dosing in adult patients with various indications of warfarin use.

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Section: [ 1 4 8 # 3 C H E S T S E P T E M B E R 2 0 1 5 ]mentioning

confidence: 99%

Meta-analysis of Randomized Controlled Trials of Genotype-Guided vs Standard Dosing of Warfarin

Dahal

Sharma

Fung

et al. 2015

CHEST

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“…Whereas GGCX produces Gla residues in the substrate protein, the co-substrate of GGCX, vitamin K hydroquinone (vit KH2), is oxygenated into vitamin K 2,3-epoxide (vit KϾO) (9) (Fig. 1).…”

mentioning

confidence: 99%

VKORC1L1, an Enzyme Rescuing the Vitamin K 2,3-Epoxide Reductase Activity in Some Extrahepatic Tissues during Anticoagulation Therapy

Hammed

Matagrin

Spohn

et al. 2013

Journal of Biological Chemistry

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Background: Effective involvement of VKORC1L1 in vitamin K epoxide reductase activity, target of vitamin K antagonists (VKAs), is still unclear. Results: VKORC1L1 is not inhibited by VKAs and catalyzes VKOR activity in extrahepatic tissues. Conclusion: During long term anticoagulation the limited unwanted side effects of VKAs are due to VKORC1L1. Significance: Potential pharmaco-toxicologic effects of specific VKORC1L1 inhibitors should be assessed.

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“…However, along with the fact that systemically administered antioxidant effects of green tea reduce the incident of dental caries, vitamin K2 may prove to be an even more potent antioxidant [20][21][22][23][24].…”

Section: A Systemic Approach and The Impact Of Oxidation Controlmentioning

confidence: 99%

“…Hence, it can be construed that there exists a close relationship between both of these exocrine/endocrine glands through the hypothalamus. High levels of vitamin K2 are also located in the brain, heart, and bone [40,41] which definitely is of significance for many disease states, including dental caries, which has been shown to be associated with oxidative stress [6,24].…”

Section: A Summary Of the Features Of Vitamin K2mentioning

confidence: 99%

Vitamin K2 and its Impact on Tooth Epigenetics

Gordeladze¹,

Landin²,

Johnsen³

et al. 2017

Vitamin K2 - Vital for Health and Wellbeing

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The impact of nutritional signals plays an important role in systemic-based «models» of dental caries. Present hypotheses now focus both on the oral environment and other organs, like the nervous system and brain. The tooth is subjected to shear forces, nourishing and cleansing, and its present "support system" (the hypothalamus/parotid axis) relays endocrine signaling to the parotid gland. Sugar consumption enhances hypothalamic oxidative stress (ROS), reversing dentinal fluid flow, thus creating an enhanced vulnerability to the oral bacterial flora. The acid, produced by the oral bacterial flora, then leads to erosion of the dentine, and an irreversible loss of dental enamel layers. This attack brings about inflammatory responses, yielding metalloproteinase-based "dissolution". However, vitamin K2 (i.e. MK-4/MK-7) may come to the rescue with its antioxidant property, locally (mouth cavity) or systemically (via the brain), thus sustaining/preserving hormone-induced dentinal fluid flow (encompassing oxidative stress) and boosting/magnifying bodily inflammatory responses. However, sugars may also reduce the tooth's natural defences through endocrine signaling, thus enhancing acid-supported enamel dentine erosion. Vitamin K2 sustains and improves the salivary buffering capacity via its impact on the secretion/flow of calcium and inorganic phosphates. Interestingly, primitive cultures' diets (low-sugar and high-K2 diets) preserve dental health.

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The Vitamin K Cycle

Cited by 153 publications

References 129 publications

Meta-analysis of Randomized Controlled Trials of Genotype-Guided vs Standard Dosing of Warfarin

Meta-analysis of Randomized Controlled Trials of Genotype-Guided vs Standard Dosing of Warfarin

VKORC1L1, an Enzyme Rescuing the Vitamin K 2,3-Epoxide Reductase Activity in Some Extrahepatic Tissues during Anticoagulation Therapy

Vitamin K2 and its Impact on Tooth Epigenetics

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