Vascular calcification: the price to pay for anticoagulation therapy with vitamin K-antagonists |
| |
Authors: | Chatrou Martijn L L Winckers Kristien Hackeng Tilman M Reutelingsperger Chris P Schurgers Leon J |
| |
Affiliation: | Department of Biochemistry, Cardiovascular Research Institute Maastricht, MUMC, Maastricht, The Netherlands. |
| |
Abstract: | Vitamin K-antagonists (VKA) are the most widely used anti-thrombotic drugs with substantial efficacy in reducing risk of arterial and venous thrombosis. Several lines of evidence indicate, however, that VKA inhibit not only post-translational activation of vitamin K-dependent coagulation factors but also synthesis of functional extra-hepatic vitamin K-dependent proteins thereby eliciting undesired side-effects. Vascular calcification is one of the recently revealed side-effects of VKA. Vascular calcification is an actively regulated process involving vascular cells and a number of vitamin K-dependent proteins. Mechanistic understanding of vascular calcification is essential to improve VKA-based treatments of both thrombotic disorders and atherosclerosis. This review addresses vitamin K-cycle and vitamin K-dependent processes of vascular calcification that are affected by VKA. We conclude that there is a growing need for better understanding of the effects of anticoagulants on vascular calcification and atherosclerosis. |
| |
Keywords: | VKA, vitamin K antagonists MGP, matrix Gla protein GGCX, γ-glutamylcarboxylase, enzyme responsible for carboxylation Gla, γ-carboxyglutamic acid or γ-carboxyglutamate Glu, glutamic acid VKDP, vitamin K-dependent proteins K, vitamin K-quinone KH2, vitamin K hydro-quinone KO, vitamin K 2,3-epoxide VKOR, vitamin K-epoxide reductase, reducing enzyme for KH2 DT-diaphorase, quinone oxidoreductase, reducing enzyme for KH2 VKORC1, VKOR complex 1 CYP2C9, Cytochrome P450 2C9, cytochrome responsible for VKA metabolism HDN, hemorrhagic disease of the newborn VKDB, vitamin K-deficiency bleeding OC, osteocalcin Gas-6, growth arrest specific gene 6 protein VSMCs, vascular smooth muscle cells PCS, peak circumferential stress ECM, extracellular matrix MV, matrix vesicles, membrane shedded vesicles derived from viable cells AB, apoptotic bodies, vesicular cell remnants of apoptotic cells MSCT, multi-slice computed tomography PIVKA-II, Protein Induced by Vitamin K Absence of Antagonism-Factor II PARs, protease activated receptors NOAC, novel oral anticoagulants |
本文献已被 ScienceDirect PubMed 等数据库收录! |
|