ArticleScientific reports2018
Missense mutation of VKORC1 leads to medial arterial calcification in rats.
Article in Scientific reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 11 citations in OpenAlex.
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- Possible contribution of phosphate to the pathogenesis of chronic kidney disease in dolphins.Scientific reports · 2023Article
- Relationship between Structure and Biological Activity of Various Vitamin K Forms.Foods (Basel, Switzerland) · 2021Review
- Review
- Monckeberg's Medial Sclerosis as a Cause for Headache and Facial Pain.Current pain and headache reports · 2021Review
- Biomarkers Potency to Monitor Non-target Fauna Poisoning by Anticoagulant Rodenticides.Frontiers in veterinary science · 2020Review
- Establishment of the Variation of Vitamin K Status According toNutrients · 2019Article
- The Role of Vitamin K and Its Related Compounds in Mendelian and Acquired Ectopic Mineralization Disorders.International journal of molecular sciences · 2019Review
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Vitamin K plays a crucial role in the regulation of vascular calcifications by allowing activation of matrix Gla protein. The dietary requirement for vitamin K is low because of an efficient recycling of vitamin K by vitamin K epoxide reductase (VKORC1). However, decreased VKORC1 activity may result in vascular calcification. More than 30 coding mutations of VKORC1 have been described. While these mutations have been suspected of causing anticoagulant resistance, their association with an increase in the risk of vascular calcification has never been considered. We thus investigated functional cardiovascular characteristics in a rat model mutated in VKORC1. This study revealed that limited intake in vitamin K in mutated rat induced massive calcified areas in the media of arteries of lung, aortic arch, kidneys and testis. Development of calcifications could be inhibited by vitamin K supplementation. In calcified areas, inactive Matrix Gla protein expression increased, while corresponding mRNA expression was not modified. Mutation in VKORC1 associated with a limited vitamin K intake is thus a major risk for cardiovascular disease. Our model is the first non-invasive rat model that shows spontaneous medial calcifications and would be useful for studying physiological function of vitamin K.
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