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Wessel S Rodenburg Molecular Cell Biology Lab at Department of Molecular Hematology, Sanquin Research and Landsteiner Laboratory, Amsterdam, the Netherlands

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Jaap D van Buul Molecular Cell Biology Lab at Department of Molecular Hematology, Sanquin Research and Landsteiner Laboratory, Amsterdam, the Netherlands
Leeuwenhoek Centre for Advanced Microscopy, Section Molecular Cytology at Swammerdam Institute for Life Sciences at University of Amsterdam, Amsterdam, the Netherlands

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Rho GTPases are small signalling G-proteins that are central regulators of cytoskeleton dynamics, and thereby regulate many cellular processes, including the shape, adhesion and migration of cells. As such, Rho GTPases are also essential for the invasive behaviour of cancer cells, and thus involved in several steps of the metastatic cascade, including the extravasation of cancer cells. Extravasation, the process by which cancer cells leave the circulation by transmigrating through the endothelium that lines capillary walls, is an essential step for metastasis towards distant organs. During extravasation, Rho GTPase signalling networks not only regulate the transmigration of cancer cells but also regulate the interactions between cancer and endothelial cells and are involved in the disruption of the endothelial barrier function, ultimately allowing cancer cells to extravasate into the underlying tissue and potentially form metastases. Thus, targeting Rho GTPase signalling networks in cancer may be an effective approach to inhibit extravasation and metastasis. In this review, the complex process of cancer cell extravasation will be discussed in detail. Additionally, the roles and regulation of Rho GTPase signalling networks during cancer cell extravasation will be discussed, both from a cancer cell and endothelial cell point of view.

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Elisabeth Kugler Department of Infection, Immunity and Cardiovascular Disease, University of Sheffield, Medical School, Sheffield, UK
The Bateson Centre, Firth Court, University of Sheffield, Western Bank, Sheffield, UK
Insigneo Institute for in silico Medicine, Sheffield, UK
Institute of Ophthalmology, Faculty of Brain Sciences, University College London, London, UK

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Ryan Snodgrass Department of Infection, Immunity and Cardiovascular Disease, University of Sheffield, Medical School, Sheffield, UK
The Bateson Centre, Firth Court, University of Sheffield, Western Bank, Sheffield, UK

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George Bowley Department of Infection, Immunity and Cardiovascular Disease, University of Sheffield, Medical School, Sheffield, UK
The Bateson Centre, Firth Court, University of Sheffield, Western Bank, Sheffield, UK

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Karen Plant Department of Infection, Immunity and Cardiovascular Disease, University of Sheffield, Medical School, Sheffield, UK
The Bateson Centre, Firth Court, University of Sheffield, Western Bank, Sheffield, UK

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Jovana Serbanovic-Canic Department of Infection, Immunity and Cardiovascular Disease, University of Sheffield, Medical School, Sheffield, UK
The Bateson Centre, Firth Court, University of Sheffield, Western Bank, Sheffield, UK

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Noémie Hamilton Department of Infection, Immunity and Cardiovascular Disease, University of Sheffield, Medical School, Sheffield, UK
The Bateson Centre, Firth Court, University of Sheffield, Western Bank, Sheffield, UK

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Paul C Evans Department of Infection, Immunity and Cardiovascular Disease, University of Sheffield, Medical School, Sheffield, UK
The Bateson Centre, Firth Court, University of Sheffield, Western Bank, Sheffield, UK
Insigneo Institute for in silico Medicine, Sheffield, UK

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Timothy Chico Department of Infection, Immunity and Cardiovascular Disease, University of Sheffield, Medical School, Sheffield, UK
The Bateson Centre, Firth Court, University of Sheffield, Western Bank, Sheffield, UK

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Paul Armitage Department of Infection, Immunity and Cardiovascular Disease, University of Sheffield, Medical School, Sheffield, UK
Insigneo Institute for in silico Medicine, Sheffield, UK

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The role of blood flow in vascular development is complex and context-dependent. In this study, we quantify the effect of the lack of blood flow on embryonic vascular development on two vascular beds, namely the cerebral and trunk vasculature in zebrafish. We perform this by analysing vascular topology, endothelial cell (EC) number, EC distribution, apoptosis, and inflammatory response in animals with normal blood flow or absent blood flow. We find that absent blood flow reduced vascular area and EC number significantly in both examined vascular beds, but the effect is more severe in the cerebral vasculature, and severity increases over time. Absent blood flow leads to an increase in non-EC-specific apoptosis without increasing tissue inflammation, as quantified by cerebral immune cell numbers and nitric oxide. Similarly, while stereotypic vascular patterning in the trunk is maintained, intra-cerebral vessels show altered patterning, which is likely to be due to vessels failing to initiate effective fusion and anastomosis rather than sprouting or path-seeking. In conclusion, blood flow is essential for cellular survival in both the trunk and cerebral vasculature, but particularly intra-cerebral vessels are affected by the lack of blood flow, suggesting that responses to blood flow differ between these two vascular beds.

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Sara Sileno Istituto Dermopatico dell’Immacolata, IDI-IRCCS, Experimental Immunology Laboratory Via Monti di Creta, Rome, Italy

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Sara Beji Istituto Dermopatico dell’Immacolata, IDI-IRCCS, Experimental Immunology Laboratory Via Monti di Creta, Rome, Italy

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Marco D’Agostino Istituto Dermopatico dell’Immacolata, IDI-IRCCS, Experimental Immunology Laboratory Via Monti di Creta, Rome, Italy

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Alessandra Carassiti Istituto Dermopatico dell’Immacolata, IDI-IRCCS, Experimental Immunology Laboratory Via Monti di Creta, Rome, Italy

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Guido Melillo Unit of Cardiology, IDI-IRCCS, Via Monti di Creta, Rome, Italy

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Alessandra Magenta Institute of Translational Pharmacology (IFT), National Research Council of Italy (CNR), Via Fosso del Cavaliere, Rome, Italy

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Psoriasis is a chronic inflammatory disease involving the skin. Both genetic and environmental factors play a pathogenic role in psoriasis and contribute to the severity of the disease. Psoriasis, in fact, has been associated with different comorbidities such as diabetes, metabolic syndrome, gastrointestinal or kidney diseases, cardiovascular disease (CVD), and cerebrovascular diseases (CeVD). Indeed, life expectancy in severe psoriasis is reduced by up to 5 years due to CVD and CeVD. Moreover, patients with severe psoriasis have a higher prevalence of traditional cardiovascular (CV) risk factors, including dyslipidemia, diabetes, smoking, and hypertension. Further, systemic inflammation is associated with oxidative stress increase and induces endothelial damage and atherosclerosis progression. Different miRNA have been already described in psoriasis, both in the skin tissues and in the blood flow, to play a role in the progression of disease. In this review, we will summarize and discuss the most important miRNAs that play a role in psoriasis and are also linked to CVD.

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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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The role of mechanical forces is emerging as a new player in the pathophysiologic programming of the cardiovascular system. The ability of the cells to ‘sense’ mechanical forces does not relate only to perception of movement or flow, as intended traditionally, but also to the biophysical properties of the extracellular matrix, the geometry of the tissues, and the force distribution inside them. This is also supported by the finding that cells can actively translate mechanical cues into discrete gene expression and epigenetic programming. In the present review, we will contextualize these new concepts in the vascular pathologic programming.

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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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Cellular senescence is now recognized as one of the hallmarks of aging. Herein, we examine current findings on senescence of the vascular endothelium and its impacts on age-related vascular diseases. Endothelial senescence can result in systemic metabolic changes, implicating senescence in chronic diseases such as diabetes, obesity and atherosclerosis. Senolytics, drugs that eliminate senescent cells, afford new therapeutic strategies for control of these chronic diseases.

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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 pathophysiology of thoracic aortic aneurysm and dissection is poorly understood, despite high mortality. An evidence review was conducted to examine the biomechanical, chemical and genetic factors involved in thoracic aortic pathology. The composition of connective tissue and smooth muscle cells can mediate important mechanical properties that allow the thoracic aorta to withstand and transmit pressures. Genetic syndromes can affect connective tissue and signalling proteins that interrupt smooth muscle function, leading to tissue failure. There are complex interplaying factors that maintain thoracic aortic function in health and are disrupted in disease, signifying an area for extensive research.

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Roberta Giordo Department of Medical Laboratory Sciences, College of Health Sciences, and Sharjah Institute for Medical Research, University of Sharjah, Sharjah, United Arab Emirates

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Panagiotis Paliogiannis Department of Medical, Surgical and Experimental Surgery, University of Sassari, Sassari, Italy

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Arduino Aleksander Mangoni Discipline of Clinical Pharmacology, College of Medicine and Public Health, Flinders University and Flinders Medical Centre, Adelaide, Australia

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Gianfranco Pintus Department of Medical Laboratory Sciences, College of Health Sciences, and Sharjah Institute for Medical Research, University of Sharjah, Sharjah, United Arab Emirates
Department of Biomedical Sciences, University of Sassari, Viale San Pietro, Sassari, Italy

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SARS-CoV-2 is the agent responsible for the coronavirus disease (COVID-19), which has been declared a pandemic by the World Health Organization. The clinical evolution of COVID-19 ranges from asymptomatic infection to death. Older people and patients with underlying medical conditions, particularly diabetes, cardiovascular and chronic respiratory diseases are more susceptible to develop severe forms of COVID-19. Significant endothelial damage has been reported in COVID-19 and growing evidence supports the key pathophysiological role of this alteration in the onset and the progression of the disease. In particular, the impaired vascular homeostasis secondary to the structural and functional damage of the endothelium and its main component, the endothelial cells, contributes to the systemic proinflammatory state and the multiorgan involvement observed in COVID-19 patients. This review summarizes the current evidence supporting the proposition that the endothelium is a key target of SARS-CoV-2, with a focus on the molecular mechanisms involved in the interaction between SARS-CoV-2 and endothelial cells.

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Laura Monteonofrio Laboratory of Cardiovascular Science, National Institute on Aging, National Institutes of Health, Baltimore, Maryland, USA

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Maria Cristina Florio Laboratory of Cardiovascular Science, National Institute on Aging, National Institutes of Health, Baltimore, Maryland, USA

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Majd AlGhatrif Laboratory of Cardiovascular Science, National Institute on Aging, National Institutes of Health, Baltimore, Maryland, USA
Longitudinal Study Section, National Institute on Aging, National Institutes of Health, Baltimore, Maryland, USA
Division of Cardiology, The Johns Hopkins University School of Medicine, Baltimore, Maryland, USA

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Edward G Lakatta 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, The Johns Hopkins University School of Medicine, Baltimore, Maryland, USA

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Coronavirus disease 2019 (COVID-19) is a new infectious disease caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). COVID-19 is frequently characterized by a marked inflammatory response with severe pneumonia and respiratory failure associated with multiorgan involvement. Some risk factors predispose patients to develop a more severe infection and to an increased mortality; among them, advanced age and male gender have been identified as major and independent risk factors for COVID-19 poor outcome. The renin-angiotensin-aldosterone system (RAAS) is strictly involved in COVID-19 because angiotensin converting enzyme 2 (ACE2) is the host receptor for SARS-CoV-2 and also converts pro-inflammatory angiotensin (Ang) II into anti-inflammatory Ang(1–7). In this review, we have addressed the effect of aging and gender on RAAS with emphasis on ACE2, pro-inflammatory Ang II/Ang II receptor 1 axis and anti-inflammatory Ang(1–7)/Mas receptor axis.

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Dwitiya Sawant Center for Cardiovascular Research and The Heart Center, Nationwide Children’s Hospital, Columbus, Ohio, USA

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Brenda Lilly Center for Cardiovascular Research and The Heart Center, Nationwide Children’s Hospital, Columbus, Ohio, USA
Department of Pediatrics, The Ohio State University, Columbus, Ohio, USA

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miRNAs are small regulatory RNAs which govern gene expression post-transcriptionally by primarily binding to the 3'-UTR of mRNA target genes. miR-145 is a well-studied miRNA that has been implicated in controlling a range of biological processes. miR-145 is expressed in a variety of tissues and cell types and acts as a tumor-suppressor by regulating target gene signaling pathways involved in different aspects of tumor growth and progression. There is also strong evidence that highlights the important functions of miR-145 in the cardiovascular system. Here, we review the mechanisms of miR-145 in tumorigenesis and cancer progression and compare and contrast with the roles of miR-145 in cardiovascular development and disease. We discuss the important targets of miR-145 in cancer and their possible link to the cardiovascular system.

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Abdallah Al-Mohammad Department of Infection, Immunity and Cardiovascular Diseases, University of Sheffield, Sheffield, UK
Sheffield Teaching Hospitals NHS Foundation Trust, Sheffield, UK

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David G Partridge Sheffield Teaching Hospitals NHS Foundation Trust, Sheffield, UK
Florey Institute for Host Pathogen Research, University of Sheffield, Sheffield, UK

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Graham Fent Sheffield Teaching Hospitals NHS Foundation Trust, Sheffield, UK

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Oliver Watson Sheffield Teaching Hospitals NHS Foundation Trust, Sheffield, UK

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Nigel T Lewis Sheffield Teaching Hospitals NHS Foundation Trust, Sheffield, UK

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Robert F Storey Department of Infection, Immunity and Cardiovascular Diseases, University of Sheffield, Sheffield, UK
Sheffield Teaching Hospitals NHS Foundation Trust, Sheffield, UK

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Michael Makris Department of Infection, Immunity and Cardiovascular Diseases, University of Sheffield, Sheffield, UK
Sheffield Teaching Hospitals NHS Foundation Trust, Sheffield, UK

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Timothy J Chico Department of Infection, Immunity and Cardiovascular Diseases, University of Sheffield, Sheffield, UK
Sheffield Teaching Hospitals NHS Foundation Trust, Sheffield, UK

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Abstract

Since the first description of COVID-19 in December 2019, more than 63,000 publications have described its virology, clinical course, management, treatment and prevention. Most physicians are now encountering, or will soon encounter, patients with COVID-19 and must attempt to simultaneously assimilate this avalanche of information while managing an entirely novel disease with few guiding precedents. It is increasingly clear that, although primarily a respiratory illness, COVID-19 is associated with cardiovascular complications. However, the true incidence of direct cardiac complications remains unclear, as all complications thus far reported can also occur in patients without COVID-19. In this review, we briefly summarise and critically appraise the data on cardiac complications associated with COVID-19 and describe some cases from our own experience. We identify unresolved questions and highlight the many uncertainties in this developing field.

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