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Miesje M van der Stoel Amsterdam UMC, University of Amsterdam, location AMC, Amsterdam Cardiovascular Sciences, Department of Medical Biochemistry, Meibergdreef, Amsterdam, The Netherlands

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Maria P Kotini Biozentrum der Universität Basel, Spitalstrasse, Basel, Switzerland

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Rianne M Schoon Amsterdam UMC, University of Amsterdam, location AMC, Amsterdam Cardiovascular Sciences, Department of Medical Biochemistry, Meibergdreef, Amsterdam, The Netherlands

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Markus Affolter Biozentrum der Universität Basel, Spitalstrasse, Basel, Switzerland

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Heinz-Georg Belting Biozentrum der Universität Basel, Spitalstrasse, Basel, Switzerland

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Stephan Huveneers Amsterdam UMC, University of Amsterdam, location AMC, Amsterdam Cardiovascular Sciences, Department of Medical Biochemistry, Meibergdreef, Amsterdam, The Netherlands

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mechanotransduction complex ( 15 , 16 , 17 , 18 ). The interaction of the VE–cadherin–catenin complex with the actin cytoskeleton stabilises the AJs and maintains endothelial monolayer integrity ( 19 , 20 , 21 ). Tension on the VE–cadherin complex results in

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DOI:
https://doi.org/10.1530/VB-22-0012
Volume/Issue:
Volume 5: Issue 1
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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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.vph.2018.06.013 ) 12 Garoffolo G Pesce M . Mechanotransduction in the cardiovascular system: From developmental origins to homeostasis and pathology . Cells 2019 8 1607 . ( https://doi.org/10.3390/cells8121607 ) 13 Garoffolo G Ferrari S

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https://doi.org/10.1530/VB-21-0002
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Volume 3: Issue 1
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Cristina Caffarra Malvezzi Department of Medicine and Surgery, University of Parma, Parma, Italy

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Aderville Cabassi Department of Medicine and Surgery, University of Parma, Parma, Italy

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Michele Miragoli Department of Medicine and Surgery, University of Parma, Parma, Italy
Center of Excellence for Toxicological Research, Department of Medicine and Surgery, University of Parma, Parma, Italy
Department of Cardiovascular Medicine, Humanitas Clinical and Research Center - IRCCS, 20090 Rozzano, Milan, Italy

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the entire body ( 1 ). One of those physiological processes is the mechano-transduction that, via several actors like stretch-activated channels (SACS ( 2 )), the sarcoplasmic reticulum (SR) ( 3 ), ryanodine receptor (RyR ( 4 )), structural proteins

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https://doi.org/10.1530/VB-20-0002
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Volume 2: Issue 1
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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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Spring Harbor Perspectives in Biology 2011 3 a005074 . ( https://doi.org/10.1101/cshperspect.a005074 ) 17 Elosegui-Artola A Trepat X Roca-Cusachs P . Control of mechanotransduction by molecular clutch dynamics . Trends in Cell Biology

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https://doi.org/10.1530/VB-20-0007
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Volume 2: Issue 1
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Ryan von Kleeck Department of Systems Pharmacology and Translational Therapeutics, University of Pennsylvania, Philadelphia Pennsylvania, USA
Center for Engineering MechanoBiology, University of Pennsylvania, Philadelphia, Pennsylvania, USA

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Paola Castagnino Department of Systems Pharmacology and Translational Therapeutics, University of Pennsylvania, Philadelphia Pennsylvania, USA
Institute of Translational Medicine and Therapeutics, University of Pennsylvania, Philadelphia, Pennsylvania, USA

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Richard K Assoian Department of Systems Pharmacology and Translational Therapeutics, University of Pennsylvania, Philadelphia Pennsylvania, USA
Center for Engineering MechanoBiology, University of Pennsylvania, Philadelphia, Pennsylvania, USA
Institute of Translational Medicine and Therapeutics, University of Pennsylvania, Philadelphia, Pennsylvania, USA

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multifunctionality . Journal of Cell Biology 2015 208 11 – 22 . ( https://doi.org/10.1083/jcb.201409047 ) 10.1083/jcb.201409047 12 Dahl KN Ribeiro AJS Lammerding J . Nuclear shape, mechanics, and mechanotransduction . Circulation Research 2008 102 1307

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https://doi.org/10.1530/VB-21-0018
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Volume 4: Issue 1
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Sashini Iddawela Department of Respiratory Medicine, University Hospitals Birmingham, Birmingham, UK

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Andrew Ravendren School of Medicine, Imperial College London, London, UK

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Amer Harky Department of Cardiothoracic Surgery, Liverpool Heart and Chest Hospital, Liverpool, UK

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. The factors governing genetic syndromes such as abnormal elastin, tone and signalling can lead to maladaptive mechanotransduction which ultimately lead to a failure in aortic tissue to cope with wall stress. Since the genetic basis of TAAD is poorly

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https://doi.org/10.1530/VB-20-0015
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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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flow are an essential environmental factor that activate the vascular endothelium. However, in addition to mechanotransduction properties, flow also directs secondary effects associated with chemical signaling, such as, for example, the transport of

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https://doi.org/10.1530/VB-19-0031
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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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–mesenchymal transition in response to FSS ( 19 ). In addition to the shear forces, mechanical forces of perfusion also include the mechanical stretching of ECs caused by vasodilation. Lorenz et al. found that blood perfusion leads to mechanotransduction in hepatic

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https://doi.org/10.1530/VB-22-0001
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Volume 4: Issue 1
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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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1, impacting SMC mechanotransduction and thus affecting various signalling pathways of ECM metabolism, resulting in deleterious effect of hemostasis and homeostasis ( 69 , 70 ). Loss of tensile capacity occurs as GAGs displace elastic fibres

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https://doi.org/10.1530/VB-19-0027
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Volume 1: Issue 1
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Aurélie Hautefort Department of Pathology and Immunology, University of Geneva, Geneva, Switzerland

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Anna Pfenniger Department of Pathology and Immunology, University of Geneva, Geneva, Switzerland
Department of Medical Specializations – Cardiology, University of Geneva, Geneva, Switzerland

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Brenda R Kwak Department of Pathology and Immunology, University of Geneva, Geneva, Switzerland
Department of Medical Specializations – Cardiology, University of Geneva, Geneva, Switzerland

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.ydbio.2011.04.004 ) 23 Sabine A Agalarov Y Maby-El Hajjami H Jaquet M Hagerling R Pollmann C Bebber D Pfenniger A Miura N Dormond O , Mechanotransduction, PROX1, and FOXC2 cooperate to control connexin37 and calcineurin during

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https://doi.org/10.1530/VB-19-0015
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Volume 1: Issue 1
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