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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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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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similarities and differences in calcific pathological development between heart valves and blood vessels. Of particular focus is the role that oscillatory blood flow patterns play in biomechanical-induced activation of diseased pathways in valvular vs vascular

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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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Paul H A Quax Vascular Surgery, Leiden University Medical Center, Leiden, The Netherlands

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Marie-José T H Goumans Cell and Chemical Biology, Leiden University Medical Center, Leiden, Netherlands

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cell types present within the (cardio)vascular system, which all are crucial players in the field, and also vascular (re)modelling, regeneration, calcification, animal models and alternative models, imaging technologies, biochemical and biomechanics

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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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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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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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Sandra Neumann Research and Imaging Centre (CRIC) Bristol, University of Bristol, Bristol, UK

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Elena G Milano UCL Institute of Cardiovascular Science and Great Ormond Street Hospital for Children, London, UK
Department of Surgery, Dentistry, Paediatrics and Gynaecology, University of Verona, Verona, Italy

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Chiara Bucciarelli-Ducci Research and Imaging Centre (CRIC) Bristol, University of Bristol, Bristol, UK
University Hospitals Bristol, NHS Foundation Trust, Bristol, UK
Bristol Medical School, University of Bristol, Bristol, UK

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Giovanni Biglino Research and Imaging Centre (CRIC) Bristol, University of Bristol, Bristol, UK
Department of Surgery, Dentistry, Paediatrics and Gynaecology, University of Verona, Verona, Italy
University Hospitals Bristol, NHS Foundation Trust, Bristol, UK
Bristol Medical School, University of Bristol, Bristol, UK

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near equivalent to that of magnetic resonance scans ( 17 ). Furthermore, DSCT allows for more accurate assessment of calcified plaque volume, as it uses two x-ray sources with different energies to achieve more detailed Hounsfield unit measurements ( 18

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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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Tomasz Jadczyk Department of Cardiology and Structural Heart Diseases, Medical University of Silesia, Katowice, Poland
Interventional Cardiac Electrophysiology Group, International Clinical Research Center, St. Anne’s University Hospital Brno, Brno, Czech Republic

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Guido Caluori Department of Cardiology and Structural Heart Diseases, Medical University of Silesia, Katowice, Poland
Nanobiotechnology, CEITEC-MU, Brno, Czech Republic

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Wojciech Wojakowski Department of Cardiology and Structural Heart Diseases, Medical University of Silesia, Katowice, Poland

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Zdenek Starek Interventional Cardiac Electrophysiology Group, International Clinical Research Center, St. Anne’s University Hospital Brno, Brno, Czech Republic
First Department of Internal Medicine, Cardioangiology, St. Anne’s University Hospital Brno, Masaryk University, Brno, Czech Republic

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Nanotechnology and stem cells hold a great clinical promise in the field of vascular therapies. Presented review provides an up-to-date summary about advances and challenges associated with these novel treatment strategies. Nanotechnology

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