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Catarina G Fonseca Instituto de Medicina Molecular João Lobo Antunes, Faculdade de Medicina, Universidade de Lisboa, Lisboa, Portugal
Instituto Superior Técnico, Universidade de Lisboa, Lisboa, Portugal

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Pedro Barbacena Instituto de Medicina Molecular João Lobo Antunes, Faculdade de Medicina, Universidade de Lisboa, Lisboa, Portugal

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Claudio A Franco Instituto de Medicina Molecular João Lobo Antunes, Faculdade de Medicina, Universidade de Lisboa, Lisboa, Portugal
Instituto de Histologia e Biologia do Desenvolvimento, Faculdade de Medicina, Universidade de Lisboa, Lisboa, Portugal

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EC behavior that is causative of disease. In this section, we will present evidence on this second class of vascular pathologies. Arteriovenous malformations One clear example of the contribution of defective EC migration for disease is in AVM

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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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resident cells including MSCs undergo dynamic changes and actively contribute to the remodeling process. Atherosclerotic vascular remodeling that underlies various cardiovascular diseases is initiated with endothelial dysfunction in response to pathogenic

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David Mellis University/BHF Centre for Cardiovascular Science, The Queen’s Medical Research Institute, University of Edinburgh, Edinburgh, UK

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Andrea Caporali University/BHF Centre for Cardiovascular Science, The Queen’s Medical Research Institute, University of Edinburgh, Edinburgh, UK

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emerging as an important regulatory principle in vascular disease. The regulation of miR-21 is crucial in vascular biology and SMADs are recruited to pri-mir-21 in a complex with the RNA helicase p68 and facilitate its DROSHA-mediated processing ( 15 , 16

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Ka Ka Ting Centre for the Endothelium Vascular Biology Program Centenary Institute, The University of Sydney, Sydney, New South Wales, Australia

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Paul Coleman Centre for the Endothelium Vascular Biology Program Centenary Institute, The University of Sydney, Sydney, New South Wales, Australia

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Yang Zhao Centre for the Endothelium Vascular Biology Program Centenary Institute, The University of Sydney, Sydney, New South Wales, Australia

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Mathew A Vadas Centre for the Endothelium Vascular Biology Program Centenary Institute, The University of Sydney, Sydney, New South Wales, Australia

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Jennifer R Gamble Centre for the Endothelium Vascular Biology Program Centenary Institute, The University of Sydney, Sydney, New South Wales, Australia

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regulation of blood fluidity, hemostasis and clotting, vascular tone, immune responses, inflammation, angiogenesis, and metabolism ( 2 ). Dysfunction of the endothelium is a major contributor to cardiovascular diseases (CVD) such as stroke, atherosclerosis

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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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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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structures and diseases. Despite these advantages, brain organoids still have several limitations that need to be improved, for example, lack of vascularization which leads to the paucity of oxygen and nutrients that induce necrosis of the brain organoids

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Makeda Stephenson Department of Biomedical Engineering, The Johns Hopkins University, Baltimore, Maryland, USA

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Daniel H Reich Department of Physics and Astronomy, The Johns Hopkins University, Baltimore, Maryland, USA

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Kenneth R Boheler Department of Biomedical Engineering, The Johns Hopkins University, Baltimore, Maryland, USA

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dysfunction can lead to vascular complications or disease, which contribute significantly to morbidity and mortality, particularly with aging ( 6 , 7 ). While animal models and primary human vSMC culture systems have contributed to our understanding of

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T Scott Bowen School of Biomedical Sciences, University of Leeds, Leeds, UK

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Stuart Egginton School of Biomedical Sciences, University of Leeds, Leeds, UK

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pharmacological treatments. In addition, other conditions have provided key insight into how normal mitochondrial function in vascular cells becomes disrupted with ageing and/or disease. What remains clear is that modulating mitochondrial properties can have

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Sarah Costantino Center for Molecular Cardiology, University of Zürich, Zürich, Switzerland

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Shafeeq A Mohammed Center for Molecular Cardiology, University of Zürich, Zürich, Switzerland

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Samuele Ambrosini Center for Molecular Cardiology, University of Zürich, Zürich, Switzerland

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Francesco Paneni Center for Molecular Cardiology, University of Zürich, Zürich, Switzerland
University Heart Center, Cardiology, University Hospital Zurich, Zürich, Switzerland
Department of Research and Education, University Hospital Zurich, Zürich, Switzerland

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secretion, low-grade inflammation foster the development of endothelial dysfunction, increased platelet reactivity, and pro-thrombotic states – all factors contributing to atherosclerotic vascular disease and CV events ( 4 ). Albeit therapeutic strategies

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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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processes are essential in vascular remodelling where structural changes to the blood vessel wall are necessary during normal physiology, aging, injury, and disease. Cells act in response to the ECM and remodel, but this process becomes impaired in vascular

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