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- W2942814807 endingPage "2142" @default.
- W2942814807 startingPage "2142" @default.
- W2942814807 abstract "Ectopic mineralization disorders comprise a broad spectrum of inherited or acquired diseases characterized by aberrant deposition of calcium crystals in multiple organs, such as the skin, eyes, kidneys, and blood vessels. Although the precise mechanisms leading to ectopic calcification are still incompletely known to date, various molecular targets leading to a disturbed balance between pro- and anti-mineralizing pathways have been identified in recent years. Vitamin K and its related compounds, mainly those post-translationally activated by vitamin K-dependent carboxylation, may play an important role in the pathogenesis of ectopic mineralization as has been demonstrated in studies on rare Mendelian diseases, but also on highly prevalent disorders, like vascular calcification. This narrative review compiles and summarizes the current knowledge regarding the role of vitamin K, its metabolism, and associated compounds in the pathophysiology of both monogenic ectopic mineralization disorders, like pseudoxanthoma elasticum or Keutel syndrome, as well as acquired multifactorial diseases, like chronic kidney disease. Clinical and molecular aspects of the various disorders are discussed according to the state-of-the-art, followed by a comprehensive literature review regarding the role of vitamin K in molecular pathophysiology and as a therapeutic target in both human and animal models of ectopic mineralization disorders." @default.
- W2942814807 created "2019-05-09" @default.
- W2942814807 creator A5036015001 @default.
- W2942814807 creator A5073151396 @default.
- W2942814807 creator A5076943191 @default.
- W2942814807 creator A5080213337 @default.
- W2942814807 date "2019-04-30" @default.
- W2942814807 modified "2023-10-18" @default.
- W2942814807 title "The Role of Vitamin K and Its Related Compounds in Mendelian and Acquired Ectopic Mineralization Disorders" @default.
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- W2942814807 doi "https://doi.org/10.3390/ijms20092142" @default.