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Xusheng Zhang Department of Cardiology, The First Central Clinical College of Tianjin Medical University, Tianjin, China
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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Zhanjun Huang Department of Cardiology, Longgang People’s Hospital of Shenzhen, Shenzhen, Guangdong, China

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Xiaorong Fan Department of Cardiology, Longgang People’s Hospital of Shenzhen, Shenzhen, Guangdong, China

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Xiaoqing Tan Department of Cardiology, Longgang People’s Hospital of Shenzhen, Shenzhen, Guangdong, China

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Chengzhi Lu Department of Cardiology, The First Central Clinical College of Tianjin Medical University, Tianjin, China
Department of Cardiology, Tianjin First Central Hospital, Tianjin, China

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Jianshe Yang Department of Nuclear Medicine, Shanghai Tenth People’s Hospital, Tongji University, Shanghai, 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

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Xuechong Hong Department of Cardiac Surgery, Boston Children’s Hospital, Boston, Massachusetts, USA
Department of Surgery, Harvard Medical School, Boston, Massachusetts, USA

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Wenduo Gu Cardiovascular Division, BHF Centre for Vascular Regeneration, King’s College London, London, UK

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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

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Manisha S Patil Heart Research Institute, Sydney, Australia
Faculty of Medicine and Health, University of Sydney, Sydney, Australia

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Siân P Cartland Heart Research Institute, Sydney, Australia
Faculty of Medicine and Health, University of Sydney, Sydney, Australia

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Mary M Kavurma Heart Research Institute, Sydney, Australia
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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Gloria Garoffolo Unità di Ingegneria Tissutale Cardiovascolare, Centro Cardiologico Monzino, IRCCS, Via Parea, Milan, Italy

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Maurizio Pesce Unità di Ingegneria Tissutale Cardiovascolare, Centro Cardiologico Monzino, IRCCS, Via Parea, Milan, Italy

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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

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Dai Yamanouchi Department of Surgery, Division of Vascular Surgery, University of Wisconsin School of Medicine and Public Health, Madison, Wisconsin, USA
Department of Vascular Surgery, Fujita Health University, Toyoake City, Japan

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Kimihiro Igari Department of Surgery, Division of Vascular Surgery, University of Wisconsin School of Medicine and Public Health, Madison, Wisconsin, USA

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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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Ornella Colpani IRCCS MultiMedica, Milan, Italy

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Gaia Spinetti IRCCS MultiMedica, Milan, Italy

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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

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Xiaojing Ma Department of Physiology and Pathophysiology, School of Basic Medical Sciences, Peking University, Beijing, China
Key Laboratory of Molecular Cardiovascular Science, Ministry of Education, Beijing, China

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Hongfei Li Department of Biological Sciences, Mount Holyoke College, South Hadley, Massachusetts, USA

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Shuntian Zhu Department of Physiology and Pathophysiology, School of Basic Medical Sciences, Peking University, Beijing, China
Key Laboratory of Molecular Cardiovascular Science, Ministry of Education, Beijing, China

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Zixuan Hong Department of Physiology and Pathophysiology, School of Basic Medical Sciences, Peking University, Beijing, China
Key Laboratory of Molecular Cardiovascular Science, Ministry of Education, Beijing, China

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Weijing Kong Department of Physiology and Pathophysiology, School of Basic Medical Sciences, Peking University, Beijing, China
Key Laboratory of Molecular Cardiovascular Science, Ministry of Education, Beijing, China

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Qihang Yuan Department of Physiology and Pathophysiology, School of Basic Medical Sciences, Peking University, Beijing, China
Key Laboratory of Molecular Cardiovascular Science, Ministry of Education, Beijing, China

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Runlong Wu Department of Physiology and Pathophysiology, School of Basic Medical Sciences, Peking University, Beijing, China
Key Laboratory of Molecular Cardiovascular Science, Ministry of Education, Beijing, China

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Zihang Pan Department of Physiology and Pathophysiology, School of Basic Medical Sciences, Peking University, Beijing, China
Key Laboratory of Molecular Cardiovascular Science, Ministry of Education, Beijing, China

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Jing Zhang Department of Pulmonary and Critical Care Medicine, Peking University Third Hospital, Beijing, China

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Yahong Chen Department of Pulmonary and Critical Care Medicine, Peking University Third Hospital, Beijing, China

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Xi Wang Department of Biological and Environmental Engineering, Cornell University, Ithaca, New York, USA

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Kai Wang Department of Physiology and Pathophysiology, School of Basic Medical Sciences, Peking University, Beijing, China
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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Amer Harky Department of Cardiothoracic Surgery, Liverpool Heart and Chest, Liverpool, UK

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Ka Siu Fan St. George’s Medical School, University of London, London, UK

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Ka Hay Fan Faculty of Medicine, Imperial College London, London, UK

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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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Alessandra Magenta Istituto Dermopatico dell’Immacolata, IDI-IRCCS, Rome, Italy

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Reggio Lorde Bristol Medical School (Translational Health Sciences), Bristol Heart Institute, University of Bristol, Bristol, UK

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Sunayana Begum Syed Laboratory of Cardiovascular Science, National Institute on Aging, National Institutes of Health, Baltimore, Maryland, USA

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Maurizio C Capogrossi Laboratory of Cardiovascular Science, National Institute on Aging, National Institutes of Health, Baltimore, Maryland, USA
Division of Cardiology, Johns Hopkins Bayview Medical Center, Baltimore, Maryland, USA

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Annibale Puca Ageing Unit, IRCCS MultiMedica, Milan, Italy
Department of Medicine, Surgery and Dentistry, ‘Scuola Medica Salernitana’ University of Salerno, Baronissi, Italy

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Paolo Madeddu Bristol Medical School (Translational Health Sciences), Bristol Heart Institute, University of Bristol, Bristol, UK

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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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Chia-Pei Denise Hsu Engineering Center, Department of Biomedical Engineering, Florida International University, Miami, Florida, USA

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Joshua D Hutcheson Engineering Center, Department of Biomedical Engineering, Florida International University, Miami, Florida, USA

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Sharan Ramaswamy Engineering Center, Department of Biomedical Engineering, Florida International University, Miami, Florida, USA

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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

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