Warfarin-Induced Calcification: Potential Prevention and Treatment Strategies

Warfarin is clinically used as the first choice for long-term anticoagulant therapy, and for the prevention of thromboembolic events. However, when used at low doses in the long term or high doses in the short term, warfarin treatment may result in tissue calcifications—such as calcifications in the...

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Main Authors: Xiaowu Wang, Langang Peng, Jipeng Ma, Liyun Zhang, Jincheng Liu
Format: Article
Language:English
Published: IMR Press 2022-09-01
Series:Reviews in Cardiovascular Medicine
Subjects:
Online Access:https://www.imrpress.com/journal/RCM/23/9/10.31083/j.rcm2309322
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author Xiaowu Wang
Langang Peng
Jipeng Ma
Liyun Zhang
Jincheng Liu
author_facet Xiaowu Wang
Langang Peng
Jipeng Ma
Liyun Zhang
Jincheng Liu
author_sort Xiaowu Wang
collection DOAJ
description Warfarin is clinically used as the first choice for long-term anticoagulant therapy, and for the prevention of thromboembolic events. However, when used at low doses in the long term or high doses in the short term, warfarin treatment may result in tissue calcifications—such as calcifications in the coronary arteries, peripheral vascular system, blood vessels of patients with atrial fibrillation and chronic kidney disease, and vascular valves—and atherosclerotic plaque calcification. These warfarin-induced calcifications may affect cardiovascular function and exacerbate diseases such as diabetes and hypertension. Studies have shown that quercetin, osteoprotegerin, sclerosin, and sodium thiosulfate may alleviate these effects by interfering in the Wnt/β-catenin, TG2/β-catenin, Bone Morphogenetic Protein 2 (BMP2), and Eicosapentaenoic Acid/Matrix Metallopeptidase-9 (EPA/MMP-9) pathways, respectively. Nevertheless, the mechanism underlying warfarin-induced calcification remains unknown. Therefore, the question as to how to effectively attenuate the calcification induced by warfarin and ensure its anticoagulant effect remains an urgent clinical problem that needs to be resolved. To utilize warfarin rationally and to effectively attenuate the calcifications, we focused on the clinical phenomena, molecular mechanisms, and potential strategies to prevent calcification. Highlighting these aspects could provide new insights into the effective utilization of warfarin and the reduction of its associated calcification effects.
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spelling doaj.art-bc8c95d77bf848d2ae0215eb8d4949a92022-12-22T03:47:49ZengIMR PressReviews in Cardiovascular Medicine1530-65502022-09-0123932210.31083/j.rcm2309322S1530-6550(22)00597-XWarfarin-Induced Calcification: Potential Prevention and Treatment StrategiesXiaowu Wang0Langang Peng1Jipeng Ma2Liyun Zhang3Jincheng Liu4Cardiovascular Surgery, Xijing Hospital, Fourth Military Medical University, 710032 Xi'an, Shaanxi, ChinaCardiovascular Surgery, Xijing Hospital, Fourth Military Medical University, 710032 Xi'an, Shaanxi, ChinaCardiovascular Surgery, Xijing Hospital, Fourth Military Medical University, 710032 Xi'an, Shaanxi, ChinaCardiovascular Surgery, Xijing Hospital, Fourth Military Medical University, 710032 Xi'an, Shaanxi, ChinaCardiovascular Surgery, Xijing Hospital, Fourth Military Medical University, 710032 Xi'an, Shaanxi, ChinaWarfarin is clinically used as the first choice for long-term anticoagulant therapy, and for the prevention of thromboembolic events. However, when used at low doses in the long term or high doses in the short term, warfarin treatment may result in tissue calcifications—such as calcifications in the coronary arteries, peripheral vascular system, blood vessels of patients with atrial fibrillation and chronic kidney disease, and vascular valves—and atherosclerotic plaque calcification. These warfarin-induced calcifications may affect cardiovascular function and exacerbate diseases such as diabetes and hypertension. Studies have shown that quercetin, osteoprotegerin, sclerosin, and sodium thiosulfate may alleviate these effects by interfering in the Wnt/β-catenin, TG2/β-catenin, Bone Morphogenetic Protein 2 (BMP2), and Eicosapentaenoic Acid/Matrix Metallopeptidase-9 (EPA/MMP-9) pathways, respectively. Nevertheless, the mechanism underlying warfarin-induced calcification remains unknown. Therefore, the question as to how to effectively attenuate the calcification induced by warfarin and ensure its anticoagulant effect remains an urgent clinical problem that needs to be resolved. To utilize warfarin rationally and to effectively attenuate the calcifications, we focused on the clinical phenomena, molecular mechanisms, and potential strategies to prevent calcification. Highlighting these aspects could provide new insights into the effective utilization of warfarin and the reduction of its associated calcification effects.https://www.imrpress.com/journal/RCM/23/9/10.31083/j.rcm2309322warfarinanticoagulationcalcificationprevention
spellingShingle Xiaowu Wang
Langang Peng
Jipeng Ma
Liyun Zhang
Jincheng Liu
Warfarin-Induced Calcification: Potential Prevention and Treatment Strategies
Reviews in Cardiovascular Medicine
warfarin
anticoagulation
calcification
prevention
title Warfarin-Induced Calcification: Potential Prevention and Treatment Strategies
title_full Warfarin-Induced Calcification: Potential Prevention and Treatment Strategies
title_fullStr Warfarin-Induced Calcification: Potential Prevention and Treatment Strategies
title_full_unstemmed Warfarin-Induced Calcification: Potential Prevention and Treatment Strategies
title_short Warfarin-Induced Calcification: Potential Prevention and Treatment Strategies
title_sort warfarin induced calcification potential prevention and treatment strategies
topic warfarin
anticoagulation
calcification
prevention
url https://www.imrpress.com/journal/RCM/23/9/10.31083/j.rcm2309322
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AT langangpeng warfarininducedcalcificationpotentialpreventionandtreatmentstrategies
AT jipengma warfarininducedcalcificationpotentialpreventionandtreatmentstrategies
AT liyunzhang warfarininducedcalcificationpotentialpreventionandtreatmentstrategies
AT jinchengliu warfarininducedcalcificationpotentialpreventionandtreatmentstrategies