Department of Cardiology, Tianjin First Central Hospital, Tianjin, China
Department of Cardiology, Longgang People’s Hospital of Shenzhen, Shenzhen, Guangdong, China
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Department of Cardiology, Tianjin First Central Hospital, Tianjin, China
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Introduction Vascular calcification is a common condition noted in aging, atherosclerosis, hypertension, diabetes, dyslipidemia, valvular heart disease, and chronic kidney disease ( 1 , 2 ). It is caused by heterotopic deposition of
Department of Surgery, Harvard Medical School, Boston, Massachusetts, USA
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and contributed to neointima formation in response to acute vascular injury. During chronic vascular injury, Gli1+ MSCs differentiated into osteoblast-like cells and accelerated vascular calcification. Inducible lineage tracing of c-Kit lineage cells
Faculty of Medicine and Health, University of Sydney, Sydney, Australia
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Faculty of Medicine and Health, University of Sydney, Sydney, Australia
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Faculty of Medicine and Health, University of Sydney, Sydney, Australia
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salts or hydroxyapatite in the vascular wall (vascular calcification) not only contributes to vascular stiffness but is a major risk factor for the morbidity and mortality associated with CVDs including atherosclerosis ( 85 ). As mentioned earlier, VSMCs
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example, cyclic strain induces arterial stiffening of large arteries, contributing to vascular calcification. Indeed, due to calcific plaque that affects vessel patency, the velocity of the blood flow increases with consequent effects on blood pressure
Department of Vascular Surgery, Fujita Health University, Toyoake City, Japan
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Morevati M Hogdall E Nielsen C Kjaer A Olgaard K & Lewin E . Effect of inhibition of CBP-coactivated β-catenin-mediated Wnt signaling in uremic rats with vascular calcifications . PLoS One 2018 13 e0201936. ( https://doi.org/10.1371/journal
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). On the other hand, Badi et al . showed that miR-34a is upregulated in aged murine aortas, where it promoted the senescent process and vascular calcification of VSMCs ( 24 ), a well-known complication of atherosclerosis. A recent study pointed out
Key Laboratory of Molecular Cardiovascular Science, Ministry of Education, Beijing, China
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Key Laboratory of Molecular Cardiovascular Science, Ministry of Education, Beijing, China
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Key Laboratory of Molecular Cardiovascular Science, Ministry of Education, Beijing, China
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Key Laboratory of Molecular Cardiovascular Science, Ministry of Education, Beijing, China
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Key Laboratory of Molecular Cardiovascular Science, Ministry of Education, Beijing, China
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Key Laboratory of Molecular Cardiovascular Science, Ministry of Education, Beijing, China
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Key Laboratory of Molecular Cardiovascular Science, Ministry of Education, Beijing, China
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Key Laboratory of Molecular Cardiovascular Science, Ministry of Education, Beijing, China
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on vascular calcification by inhibiting endothelial BMP/SMAD1/5 signaling . Circulation Research 2021 129 e87 – e100 . ( https://doi.org/10.1161/CIRCRESAHA.120.318690 ) 17 Hergenreider E Heydt S Tréguer K Boettger T Horrevoets AJG Zeiher
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://doi.org/10.1038/s41598-019-43322-3 ) 97 Durham AL Speer MY Scatena M Giachelli CM Shanahan CM . Role of smooth muscle cells in vascular calcification: implications in atherosclerosis and arterial stiffness . Cardiovascular Research 2018 590
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Division of Cardiology, Johns Hopkins Bayview Medical Center, Baltimore, Maryland, USA
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Department of Medicine, Surgery and Dentistry, ‘Scuola Medica Salernitana’ University of Salerno, Baronissi, Italy
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, vascular calcification, cardiac fibrosis, and adverse remodeling in heart failure. Its inhibition can improve cardiovascular repair. miRNA-21 miR-21 is epigenetically regulated in ovarian cancer and colorectal cancer ( 46 , 47 ). miRNA-21
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cell behavior due to environmental cues ( 13 ), in which loss of smooth muscle cell contractility leads to cell migration, plaque formation, and vascular calcification ( 14 ). Aortic valve stenosis occurs when valve tissues become thickened or stiff