10,729 results match your criteria Cardiovascular research[Journal]


Getting your research funded (and other tips for early career cardiovascular investigators).

Authors:
Metin Avkiran

Cardiovasc Res 2019 Apr 21. Epub 2019 Apr 21.

British Heart Foundation, Medical Directorate, Greater London House, 180 Hampstead Road, London NW1 7AW, UK.

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http://dx.doi.org/10.1093/cvr/cvz080DOI Listing

Resolvin E1 for reducing vascular calcification.

Cardiovasc Res 2019 Apr 15. Epub 2019 Apr 15.

Centre for Immunobiology, Institute of Infection, Immunity and Inflammation, College of Medical, Veterinary and Life Sciences, University of Glasgow, Glasgow G12 8TA, United Kingdom.

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https://academic.oup.com/cardiovascres/advance-article/doi/1
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http://dx.doi.org/10.1093/cvr/cvz101DOI Listing
April 2019
1 Read

Ketone Body Can Be A Fuel Substrate For Failing Heart.

Cardiovasc Res 2019 Apr 15. Epub 2019 Apr 15.

Department of Cell Biology and Molecular Medicine, Cardiovascular Research Institute, Rutgers-New Jersey Medical School, 185 South Orange Ave, Newark, NJ.

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http://dx.doi.org/10.1093/cvr/cvz104DOI Listing

The aorta can act as a site of naïve CD4+ T cell priming.

Cardiovasc Res 2019 Apr 13. Epub 2019 Apr 13.

Centre for Immunobiology, Institute of Infection, Immunity and Inflammation, College of Medical, Veterinary and Life Sciences, University of Glasgow, Glasgow, United Kingdom.

Aims: Aortic adaptive immunity plays a role in atherosclerosis; however, the precise mechanisms leading to T cell activation in the arterial wall remain poorly understood.

Methods And Results: Here, we have identified naïve T cells in the aorta of wild-type and T-cell receptor (TCR) transgenic mice and we demonstrate that naïve T cells can be primed directly in the vessel wall with both kinetics and frequency of T-cell activation found to be similar to splenic and lymphoid T cells. Aortic homing of naïve T cells is regulated at least in part by the P-selectin glycosylated ligand-1 (PSGL-1) receptor. Read More

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https://academic.oup.com/cardiovascres/advance-article/doi/1
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http://dx.doi.org/10.1093/cvr/cvz102DOI Listing
April 2019
3 Reads

TAM Receptors in Cardiovascular Disease.

Cardiovasc Res 2019 Apr 13. Epub 2019 Apr 13.

Centre for Immunobiology, Institute of Infection, Immunity and Inflammation, College of Medical, Veterinary and Life Sciences, University of Glasgow, Glasgow, United Kingdom.

The TAM receptors are a distinct family of three receptor tyrosine kinases, namely Tyro3, Axl and MerTK. Since their discovery in the early 1990s, they have been studied for their ability to influence numerous diseases, including cancer, chronic inflammatory and autoimmune disorders, and cardiovascular diseases. The TAM receptors demonstrate an ability to influence multiple aspects of cardiovascular pathology via their diverse effects on cells of both the vasculature and the immune system. Read More

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http://dx.doi.org/10.1093/cvr/cvz100DOI Listing
April 2019
1 Read

Arrhythmogenic Propensity of the Fibrotic Substrate after AF Ablation: A Longitudinal Study using MRI-Based Atrial Models.

Cardiovasc Res 2019 Apr 12. Epub 2019 Apr 12.

Division of Cardiology, Johns Hopkins University School of Medicine.

Aims: Inadequate modification of the atrial fibrotic substrate necessary to sustain reentrant drivers (RDs) may explain atrial fibrillation (AF) recurrence following failed pulmonary vein isolation (PVI). Personalized computational models of the fibrotic atrial substrate derived from late gadolinium enhanced (LGE)-MRI can be used to non-invasively determine the presence of RDs. The objective of this study is to assess the changes of the arrhythmogenic propensity of the fibrotic substrate after PVI. Read More

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http://dx.doi.org/10.1093/cvr/cvz083DOI Listing
April 2019
1 Read

The effect of diet on hypertensive pathology: is there a link via gut microbiota-driven immune-metabolism?

Cardiovasc Res 2019 Apr 5. Epub 2019 Apr 5.

Heart Failure Research Group, Baker Heart and Diabetes Institute, Melbourne, Australia.

Over the past decade, the immune system has emerged as an important component in the aetiology of hypertension. There has been a blooming interest in the contribution of the gut microbiota, the microbes that inhabit our small and large intestine, to blood pressure (BP) regulation. The gastrointestinal tract houses the largest number of immune cells in our body, thus, it is no surprise that its microbiota plays an important functional role in the appropriate development of the immune system through a coordinated sequence of events leading to immune tolerance of commensal bacteria. Read More

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https://academic.oup.com/cardiovascres/advance-article/doi/1
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http://dx.doi.org/10.1093/cvr/cvz091DOI Listing
April 2019
16 Reads

A sequential interferon gamma directed chemotactic cellular immune response determines survival and cardiac function post myocardial infarction.

Cardiovasc Res 2019 Apr 5. Epub 2019 Apr 5.

Center for Cardiology - Cardiology 1.

Aims: Myelomonocytic cells are critical in injury and healing post myocardial infarction (MI). Mechanisms of regulation, however, are incompletely understood. The aim of the study was to elucidate the role of interferon gamma (IFN-γ) in the orchestrated inflammatory response in a murine model of MI. Read More

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http://dx.doi.org/10.1093/cvr/cvz092DOI Listing
April 2019
1 Read

Coupling of the Na+/K+-ATPase to Ankyrin B controls Na+/Ca2+ exchanger activity in cardiomyocytes.

Cardiovasc Res 2019 Apr 5. Epub 2019 Apr 5.

Institute for Experimental Medical Research, Oslo University Hospital and University of Oslo, Oslo, Norway.

Aims: Ankyrin B (AnkB) is an adaptor protein that assembles Na+/K+-ATPase (NKA) and Na+/Ca2+ exchanger (NCX) in the AnkB macromolecular complex. Loss-of-function mutations in AnkB cause the AnkB syndrome in humans, characterized by ventricular arrhythmias and sudden cardiac death. It is unclear to what extent NKA binding to AnkB allows regulation of local Na+ and Ca2+ domains and hence NCX activity. Read More

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https://academic.oup.com/cardiovascres/advance-article/doi/1
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http://dx.doi.org/10.1093/cvr/cvz087DOI Listing
April 2019
1 Read

The polarity protein Scrib limits atherosclerosis development in mice.

Cardiovasc Res 2019 Apr 5. Epub 2019 Apr 5.

Institute for Cardiovascular Physiology, Goethe-University, Frankfurt, Frankfurt am Main, Germany.

Aims: The protein Scrib (Scribble 1) is known to control apico-basal polarity in epithelial cells. The role of polarity proteins in the vascular system remains poorly characterized; however, we previously reported that Scrib maintains the endothelial phenotype and directed migration. On this basis, we hypothesized that Scrib has anti-atherosclerotic functions. Read More

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http://dx.doi.org/10.1093/cvr/cvz093DOI Listing
April 2019
1 Read

Nanobiologics: a real game changer for targeted immunotherapy.

Authors:
Asif J Iqbal

Cardiovasc Res 2019 Mar 3. Epub 2019 Mar 3.

The Institute of Cardiovascular Sciences, College of Medical and Dental Sciences, University of Birmingham, Edgbaston, Birmingham, B15 2TT, UK.

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http://dx.doi.org/10.1093/cvr/cvz078DOI Listing

Pivotal role of membrane substrate transporters on the metabolic alterations in the pressure-overloaded heart.

Cardiovasc Res 2019 Apr 2. Epub 2019 Apr 2.

Department of Genetics & Cell Biology, Faculty of Health, Medicine and Life Sciences (FHML), Maastricht University, Maastricht, The Netherlands.

Cardiac pressure overload (PO), such as caused by aortic stenosis and systemic hypertension, commonly results in cardiac hypertrophy and may lead to the development of heart failure. PO-induced heart failure is among the leading causes of death worldwide, but its pathological origin remains poorly understood. Metabolic alterations are proposed to be an important contributor to PO-induced cardiac hypertrophy and failure. Read More

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http://dx.doi.org/10.1093/cvr/cvz060DOI Listing
April 2019
2 Reads

NOX4 is a major regulator of cord blood-derived endothelial colony-forming cells which promotes postischaemic revascularisation.

Cardiovasc Res 2019 Apr 1. Epub 2019 Apr 1.

Centre for Experimental Medicine, Wellcome-Wolfson Institute, Queen's University Belfast, Belfast.

Aims: Cord blood-derived endothelial colony-forming cells (CB-ECFCs) are a defined progenitor population with established roles in vascular homeostasis and angiogenesis, which possess low immunogenicity and high potential for allogeneic therapy, and are highly sensitive to regulation by reactive oxygen species (ROS). The aim of this study was to define the precise role of the major ROS-producing enzyme, NOX4 NADPH oxidase, in CB-ECFC vasoreparative function.

Methods And Results: In vitro CB-ECFC migration (scratch-wound assay) and tubulogenesis (tube length, branch number) was enhanced by phorbol 12-myristate 13-acetate (PMA)-induced superoxide in a NOX-dependent manner. Read More

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http://dx.doi.org/10.1093/cvr/cvz090DOI Listing

Shear stress makes its mark on the endothelial genome.

Cardiovasc Res 2019 Mar 29. Epub 2019 Mar 29.

University of Sheffield Medical School Sheffield, United Kingdom.

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http://dx.doi.org/10.1093/cvr/cvz088DOI Listing

Putting the pieces together using in vivo optical mapping.

Cardiovasc Res 2019 Mar 29. Epub 2019 Mar 29.

Department of Pharmacology, School of Medicine, University of California, Davis.

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https://academic.oup.com/cardiovascres/advance-article/doi/1
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http://dx.doi.org/10.1093/cvr/cvz089DOI Listing
March 2019
2 Reads
5.940 Impact Factor

Short-Term Preoperative Protein Restriction Attenuates Vein Graft Disease via Induction of Cystathionine ϒ-Lyase.

Cardiovasc Res 2019 Mar 29. Epub 2019 Mar 29.

Department of Surgery and the Heart and Vascular Center, Brigham & Women's Hospital and Harvard Medical School, Boston, MA, USA.

Aims: Therapies to prevent vein graft disease, a major problem in cardiovascular and lower extremity bypass surgeries, are currently lacking. Short-term preoperative protein restriction holds promise as an effective preconditioning method against surgical stress in rodent models, but whether it can improve vein graft patency after bypass surgery is undetermined. Here, we hypothesized that short-term protein restriction would limit vein graft disease via upregulation of cystathionine-gamma-lyase and increased endogenous production of the cytoprotective gaseous signaling molecule hydrogen sulfide. Read More

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http://dx.doi.org/10.1093/cvr/cvz086DOI Listing
March 2019
1 Read

Long noncoding RNA NEAT1 modulates immune cell functions and is suppressed in early onset myocardial infarction patients.

Cardiovasc Res 2019 Mar 29. Epub 2019 Mar 29.

Department of Cardiology, Campus Benjamin Franklin.

Background: Inflammation is a key driver of atherosclerosis and myocardial infarction (MI), and beyond proteins and microRNAs (miRs), long noncoding RNAs (lncRNAs) have been implicated in inflammation control. To obtain further information on the possible role of lncRNAs in the context of atherosclerosis, we obtained comprehensive transcriptome maps of circulating immune cells (PBMCs) of early onset MI patients. One lncRNA significantly suppressed in post-MI patients was further investigated in a murine knockout model. Read More

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http://dx.doi.org/10.1093/cvr/cvz085DOI Listing
March 2019
2 Reads

Novel findings in neutrophil biology and their impact on cardiovascular disease.

Cardiovasc Res 2019 Mar 27. Epub 2019 Mar 27.

First Clinic of Internal Medicine, Department of Internal Medicine, University of Genoa, 6 viale Benedetto XV, 16132 Genoa, Italy.

Neutrophils are the most abundant circulating leukocytes in healthy humans. These cells are central players during acute inflammatory responses, although a growing body of evidence supports a crucial role in chronic inflammation and chemokines and cytokines related to it as well. Thus, both humoral and cellular components are involved in the development of plaque formation and atherosclerosis. Read More

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https://academic.oup.com/cardiovascres/advance-article/doi/1
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http://dx.doi.org/10.1093/cvr/cvz084DOI Listing
March 2019
2 Reads

Computational fluid dynamics: can computed tomography imaging compete with cath-lab physiology?

Authors:
Mohamed Marwan

Cardiovasc Res 2019 Mar;115(4):e41-e43

Cardiology Department, Friedrich-Alexander Universität Erlangen-Nürnberg, Ulmenweg 18, Erlangen, Germany.

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http://dx.doi.org/10.1093/cvr/cvz059DOI Listing

Scientists on the Spot: Inflammation and translational research-what have we learned from the CIRT trial?

Cardiovasc Res 2019 Mar;115(4):e44-e45

Department of Molecular Physiology and Biophysics, Vanderbilt University, 2201 West End Ave, Nashville, TN, USA.

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http://dx.doi.org/10.1093/cvr/cvz047DOI Listing

Importance of quality control in 'big data': implications for statistical inference of electronic health records in clinical cardiology.

Cardiovasc Res 2019 Mar 25. Epub 2019 Mar 25.

Keele Cardiovascular Research Group, Centre for Prognosis Research, Institute for Primary Care and Health Sciences, Keele University, Stoke-on-Trent, UK.

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http://dx.doi.org/10.1093/cvr/cvy290DOI Listing

Platelets in Cardiac Ischaemia/Reperfusion Injury - A Promising Therapeutic Target.

Cardiovasc Res 2019 Mar 25. Epub 2019 Mar 25.

Atherothrombosis and Vascular Biology Laboratory, Baker Heart and Diabetes Institute, Melbourne, Victoria, Australia.

Acute myocardial infarction (AMI) is the single leading cause of mortality and morbidity worldwide. A key component of AMI therapy is the timely reopening of occluded vessels to prevent further ischaemic damage to the myocardium. However, reperfusion of the ischaemic myocardium can itself trigger reperfusion injury causing up to 50% of the overall infarct size. Read More

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http://dx.doi.org/10.1093/cvr/cvz070DOI Listing
March 2019
1 Read

The Epicardial Adipose Tissue and the Coronary Arteries: dangerous liaisons.

Cardiovasc Res 2019 Mar 23. Epub 2019 Mar 23.

Institute of Cardiology, University of Pisa, Pisa, Italy.

The adipose tissue (AT) is an endocrine organ that produces adipocytokines (adipokines), able to influence metabolic homeostasis. In the conventional classification, there are two large AT depots, characterized by different paracrine activities: the subcutaneous AT, which would mostly produce cytokines with protective properties against cardiovascular disease; and the visceral AT, responsible for the secretion of cytokines with proinflammatory, prothrombotic and proatherogenic effects. A third component, the epicardial AT (EAT) is now receiving increasing attention due to its unique anatomical and functional proximity to the myocardium and the coronary arteries. Read More

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http://dx.doi.org/10.1093/cvr/cvz062DOI Listing
March 2019
1 Read

Protease Activated Receptor 1 as potential therapeutic target in pulmonary arterial hypertension.

Cardiovasc Res 2019 Mar 23. Epub 2019 Mar 23.

Dept of Pulmonary Medicine, Erasmus MC, University Medical Center Rotterdam, Rotterdam, The Netherlands.

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http://dx.doi.org/10.1093/cvr/cvz071DOI Listing

The many facets of transcriptional regulation by HIF-1.

Cardiovasc Res 2019 Mar 20. Epub 2019 Mar 20.

Institute of Physiology, Justus Liebig University, Giessen, Germany.

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http://dx.doi.org/10.1093/cvr/cvz079DOI Listing

Cardio-oncology: a novel platform for basic and translational cardiovascular investigation driven by clinical need.

Cardiovasc Res 2019 Apr;115(5):819-823

Institute of Cardiovascular and Medical Sciences, University of Glasgow, Glasgow, UK.

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http://dx.doi.org/10.1093/cvr/cvz048DOI Listing

Adipolin/CTRP12 protects against pathological vascular remodeling through suppression of smooth muscle cell growth and macrophage inflammatory response.

Cardiovasc Res 2019 Mar 15. Epub 2019 Mar 15.

Molecular Cardiovascular Medicine, Nagoya University Graduate School of Medicine, Nagoya, Japan.

Aims: Secreted factors produced by adipose tissue are involved in the pathogenesis of cardiovascular disease. We previously identified adipolin, also known as C1q/Tnf-related protein 12, as an insulin-sensitizing adipokine. However, the role of adipolin in vascular disease remains unknown. Read More

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http://dx.doi.org/10.1093/cvr/cvz074DOI Listing
March 2019
4 Reads

Identification of a pharmacological inhibitor of Epac1 that protects the heart against acute and chronic models of cardiac stress.

Cardiovasc Res 2019 Mar 14. Epub 2019 Mar 14.

INSERM UMR-1048, Institut des Maladies Métaboliques et Cardiovasculaires, 31432 Toulouse, France.

Aims: Recent studies reported that cAMP-binding protein Epac1-deficient mice were protected against various forms of cardiac stress, suggesting that pharmacological inhibition of Epac1 could be beneficial for the treatment of cardiac diseases. To test this assumption, we characterized an Epac1-selective inhibitory compound and investigated its potential cardioprotective properties.

Methods And Results: We used the Epac1-BRET (bioluminescence resonance energy transfer) for searching for non-cyclic nucleotide Epac1 modulators. Read More

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http://dx.doi.org/10.1093/cvr/cvz076DOI Listing
March 2019
3 Reads

SGLT Receptors and Myocardial Ischemia-Reperfusion Injury: Inhibition of SGLT-1, SGLT-2 or both?

Cardiovasc Res 2019 Mar 14. Epub 2019 Mar 14.

Atherothrombosis Research Unit, Mount Sinai Heart, Icahn School of Medicine at Mount Sinai, New York, USA.

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http://dx.doi.org/10.1093/cvr/cvz077DOI Listing
March 2019
1 Read

Carbon Monoxide improves Hemodynamics during Extracorporeal Resuscitation in Pigs.

Cardiovasc Res 2019 Mar 14. Epub 2019 Mar 14.

Department of Anesthesiology and Critical Care, Medical Center - University of Freiburg.

Aims: Heart disease of different etiology remains the leading cause of cardiac arrest (CA). Despite efforts to improve the quality of cardiopulmonary resuscitation (CPR), subsequent myocardial and systemic damage after CA still present a major long-term burden. Low-dose carbon monoxide (CO) is known to exert protective effects in cardiovascular pathophysiology but clinical applications are challenged by unfavorable delivery modes. Read More

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http://dx.doi.org/10.1093/cvr/cvz075DOI Listing
March 2019
1 Read

Shining the spotlight on cardioprotection: beyond the cardiomyocyte.

Cardiovasc Res 2019 Mar 13. Epub 2019 Mar 13.

Cardiovascular & Metabolic Disorders Program, Duke-National University of Singapore Medical School, Singapore; National Heart Research Institute Singapore, National Heart Centre, Singapore; Yong Loo Lin School of Medicine, National University Singapore, Singapore; The Hatter Cardiovascular Institute, University College London, London, UK; The National Institute of Health Research University College London Hospitals Biomedical Research Centre, Research & Development, London, UK; Tecnologico de Monterrey, Centro de Biotecnologia-FEMSA, Nuevo Leon, Mexico.

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http://dx.doi.org/10.1093/cvr/cvz072DOI Listing

The Interdependent Effects of Cholesterol and Substrate Stiffness on VSMC Biomechanics.

Cardiovasc Res 2019 Mar 13. Epub 2019 Mar 13.

Division of Cardiology, Department of Medicine, Emory University, Atlanta, GA.

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http://dx.doi.org/10.1093/cvr/cvz065DOI Listing

Pentraxin 3 deficiency protects from the metabolic inflammation associated to diet-induced obesity.

Cardiovasc Res 2019 Mar 12. Epub 2019 Mar 12.

Department of Excellence of Pharmacological and Biomolecular Sciences, Università degli Studi di Milano, Milan, Italy.

Aim: Low-grade chronic inflammation characterizes obesity and metabolic syndrome. Here we aim at investigating the impact of the acute-phase protein long pentraxin 3 (PTX3) on the immune-inflammatory response occurring during diet-induced obesity.

Methods And Results: PTX3 deficiency in mice fed a high fat diet for 20 weeks protects from weight gain and adipose tissue deposition in visceral and subcutaneous depots. Read More

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http://dx.doi.org/10.1093/cvr/cvz068DOI Listing

Sialyltransferase7A promotes angiotensin II-induced cardiomyocyte hypertrophy via HIF-1α-TAK1 signaling pathway.

Cardiovasc Res 2019 Mar 11. Epub 2019 Mar 11.

Department of Physiology, Dalian Medical University, Dalian, People's Republic of China.

Aims: Sialylation is up-regulated during the development of cardiac hypertrophy. Sialyltransferase7A (Siat7A) mRNA is consistently over-expressed in the hypertrophic left ventricle of hypertensive rats independently of genetic background. The aims of this study were: (i) to detect the Siat7A protein levels and its roles in the pathological cardiomyocyte hypertrophy; (ii) to elucidate the effect of sialylation mediated by Siat7A on the transforming-growth-factor-β-activated kinase (TAK1) expression and activity in cardiomyocyte hypertrophy; (iii) to clarify hypoxia-inducible factor 1 (HIF-1) expression was regulated by Siat7A and transactivated TAK1 expression in cardiomyocyte hypertrophy. Read More

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http://dx.doi.org/10.1093/cvr/cvz064DOI Listing
March 2019
2 Reads

Nanoparticle incorporating Toll-like receptor 4 inhibitor attenuates myocardial ischaemia-reperfusion injury by inhibiting monocyte-mediated inflammation in mice.

Cardiovasc Res 2019 Mar 9. Epub 2019 Mar 9.

Department of Cardiovascular Research, Development, and Translational Research, Kyushu University, Fukuoka, Japan.

Aims: Myocardial ischaemia-reperfusion (IR) injury hampers the therapeutic effect of revascularization in patients with acute myocardial infarction. Innate immunity for damage-associated protein patterns promotes the process of IR injury; however, the blockade of Toll-like receptor 4 (TLR4) in myocardial IR injury has not been translated into clinical practice. Therefore, we aimed to examine whether the nanoparticle-mediated administration of TAK-242, a chemical inhibitor of TLR4, attenuates myocardial IR injury in a clinically feasible protocol in a mouse model. Read More

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https://academic.oup.com/cardiovascres/advance-article/doi/1
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http://dx.doi.org/10.1093/cvr/cvz066DOI Listing
March 2019
4 Reads

Protection against pressure overload-induced right heart failure by uncoupling protein 2 silencing.

Cardiovasc Res 2019 Mar 8. Epub 2019 Mar 8.

Justus-Liebig University Gießen, Department of Physiology, Aulweg 129, Gießen, Germany.

Aims: The role of uncoupling protein 2 (UCP2) in cardiac adaptation to pressure overload remains unclear. In a classical model of left ventricular pressure overload genetic deletion of UCP2 (UCP2-/-) protected against cardiac hypertrophy and failure. However, in UCP2-/- mice increased proliferation of pulmonary arterial smooth muscle cells induces mild pulmonary hypertension, right ventricular hypertrophy, and reduced cardiac output. Read More

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https://academic.oup.com/cardiovascres/advance-article/doi/1
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http://dx.doi.org/10.1093/cvr/cvz049DOI Listing
March 2019
7 Reads

The immunometabolic role of indoleamine 2 3-dioxygenase in atherosclerotic cardiovascular disease: immune homeostatic mechanisms in the artery wall.

Cardiovasc Res 2019 Mar 7. Epub 2019 Mar 7.

Cardiovascular Medicine Unit, Center for Molecular Medicine, Department of Medicine, Karolinska Institute, Karolinska University Hospital, Stockholm, Sweden.

Coronary heart disease (CHD) and stroke, the two most common cardiovascular diseases (CVDs) worldwide, are triggered by complications of atherosclerosis. Atherosclerotic plaques are triggered by a maladaptive immune response initiated by accumulation of lipids in the artery wall. Hence, disease is influenced by several non-modifiable and modifiable risk factors, including dyslipidaemia, hypertension, smoking, and diabetes. Read More

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http://dx.doi.org/10.1093/cvr/cvz067DOI Listing
March 2019
1 Read

Therapeutic modulation of RNA-binding protein Rbm38 facilitates re-endothelialization after arterial injury.

Cardiovasc Res 2019 Mar 7. Epub 2019 Mar 7.

Institute of Molecular and Translational Therapeutic Strategies (IMTTS), Hannover Medical School, Hannover, Germany.

Aims: Delayed re-endothelialization after balloon angioplasty in patients with coronary or peripheral artery disease impairs vascular healing and leads to neointimal proliferation. In the present study, we examined the effect of RNA-binding motif protein 38 (Rbm38) during re-endothelialization in a murine model of experimental vascular injury.

Methods And Results: Left common carotid arteries of C57BL/6 mice were electrically denudated and endothelial regeneration was evaluated. Read More

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http://dx.doi.org/10.1093/cvr/cvz063DOI Listing
March 2019
2 Reads
5.940 Impact Factor

Investigating and re-evaluating the role of GSK3beta kinase as a molecular target for cardioprotection by using novel pharmacological inhibitors.

Cardiovasc Res 2019 Mar 7. Epub 2019 Mar 7.

National and Kapodistrian University of Athens, Faculty of Pharmacy, Athens, Greece.

Aims: Glycogen synthase kinase 3 beta (GSK3β) link with the mitochondrial Permeability Transition Pore (mPTP) in cardioprotection is debated. We investigated the role of GSK3β in Ischemia (I)/Reperfusion (R) injury using pharmacological tools.

Methods And Results: Infarct size (IS) using the GSK3β inhibitor BIO and several novel analogues (MLS2776-MLS2779) was determined in anesthetized rabbits and mice. Read More

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http://dx.doi.org/10.1093/cvr/cvz061DOI Listing
March 2019
1 Read

Inflammation: a common contributor to cancer, aging, and cardiovascular diseases-expanding the concept of cardio-oncology.

Cardiovasc Res 2019 Apr;115(5):824-829

Division of Clinical Pharmacology, Department of Medicine IV, Center of Integrated Protein Science Munich (CIPS-M), Klinikum der Universität München, Munich, Germany.

Inflammation participates in the pathogenesis of both cancer and cardiovascular disease. This review examines the mechanistic commonalities between these two scourges of humanity through the lens of inflammation biology. Inflammatory pathways contribute to the initiation, the progression, and the complication of both malignant tumours and atherosclerotic plaques. Read More

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http://dx.doi.org/10.1093/cvr/cvz058DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6452304PMC

Toll-like Receptor 7 Deficiency Promotes Survival and Reduces Adverse Left Ventricular Remodeling After Myocardial Infarction.

Cardiovasc Res 2019 Mar 4. Epub 2019 Mar 4.

Department of Surgery, Yong Loo Lin School of Medicine, National University of Singapore, Singapore.

Aims: The Toll-like receptor 7 (TLR7) is an intracellular innate immune receptor activated by nucleic acids shed from dying cells leading to activation of the innate immune system. Since innate immune system activation is involved in the response to myocardial infarction (MI), this study aims to identify if TLR7 is involved in post-MI ischemic injury and adverse remodeling after MI.

Methods And Results: TLR7 involvement in MI was investigated in human tissue from patients with ischemic heart failure, as well as in a mouse model of permanent left anterior descending artery occlusion in C57BL/6J wild type and TLR7 deficient (TLR7-/-) mice. Read More

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http://dx.doi.org/10.1093/cvr/cvz057DOI Listing
March 2019
8 Reads

Mapping monocyte subsets to identify cardiovascular risk.

Cardiovasc Res 2019 Mar 4. Epub 2019 Mar 4.

Department of Angiocardioneurology and Translational Medicine, IRCCS Neuromed, Pozzilli, Italy.

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http://dx.doi.org/10.1093/cvr/cvz056DOI Listing

Immune cells as targets for cardioprotection: New players and novel therapeutic opportunities.

Cardiovasc Res 2019 Mar 2. Epub 2019 Mar 2.

Cardiovascular & Metabolic Disorders Program, Duke-National University of Singapore Medical School, Singapore; National Heart Research Institute Singapore, National Heart Centre, Singapore; Yong Loo Lin School of Medicine, National University Singapore, Singapore;The Hatter Cardiovascular Institute, University College London, London, UK; The National Institute of Health Research University College London Hospitals Biomedical Research Centre,Research & Development, London, UK; Tecnologico de Monterrey, Centro de Biotecnologia-FEMSA, Monterrey, NL, Mexico.

New therapies are required to reduce myocardial infarct (MI) size and prevent the onset of heart failure in patients presenting with acute myocardial infarction (AMI), one of the leading causes of death and disability globally. In this regard, the immune cell response to AMI, which comprises an initial pro-inflammatory reaction followed by an anti-inflammatory phase, contributes to final MI size and post-AMI remodelling (left ventricular (LV) size and function). The transition between these two phases is critical in this regard, with a persistent and severe pro-inflammatory reaction leading to adverse LV remodelling and increased propensity for developing heart failure. Read More

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http://dx.doi.org/10.1093/cvr/cvz050DOI Listing
March 2019
1 Read

Therapeutic gene editing, making a point.

Authors:
Anke M Smits

Cardiovasc Res 2019 Mar;115(4):e39-e40

Department of Cell and Chemical Biology, Leiden University Medical Center, 2300RC, Leiden, the Netherlands.

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http://dx.doi.org/10.1093/cvr/cvz038DOI Listing
March 2019
1 Read

Tumour necrosis factor superfamily members in ischaemic vascular diseases.

Cardiovasc Res 2019 Mar;115(4):713-720

Heart Research Institute, 7 Eliza Street, Newtown, Sydney NSW, Australia.

Current treatment of ischaemic vascular diseases such as coronary and peripheral artery disease includes angioplasty and bypass grafting, as well as lipid lowering therapies and control of other cardiovascular risk factors. Numerous members of the tumour necrosis factor superfamily (TNFSF) have recently shown emerging roles in both the protection and progression of such diseases. Understanding the role TNFSF members play in ischaemic vascular disease may provide insight into the development of novel therapeutics to prevent or treat diseases relating to atherosclerosis and ischaemia. Read More

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http://dx.doi.org/10.1093/cvr/cvz042DOI Listing
March 2019
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Cardiac innervation in acute myocardial ischaemia/reperfusion injury and cardioprotection.

Cardiovasc Res 2019 Feb 23. Epub 2019 Feb 23.

Department of Cardiology, Vascular Biology and Metabolism Area, Vall d'Hebron University Hospital and Research Institute (VHIR), Universitat Autónoma de Barcelona, Spain; Instituto CIBER de Enfermedades Cardiovasculares (CIBERCV): Instituto de Salud Carlos III, Madrid, Spain.

Acute myocardial infarction (AMI) and the heart failure (HF) that often complicates this condition, are among the leading causes of death and disability worldwide. To reduce myocardial infarct (MI) size and prevent heart failure, novel therapies are required to protect the heart against the detrimental effects of acute ischaemia/reperfusion injury (IRI). In this regard, targeting cardiac innervation may provide a novel therapeutic strategy for cardioprotection. Read More

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http://dx.doi.org/10.1093/cvr/cvz053DOI Listing
February 2019
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Vascular networking for the young at heart: Joint European Summer School for microcirculation and vascular biology.

Cardiovasc Res 2019 Mar;115(4):e49-e51

Division of Vascular Endothelium and Microcirculation, Department of Medicine III, Medical Faculty and University Clinics Carl Gustav Carus, Technische Universität Dresden, Fetscherstr. 74, D-01307 Dresden, Germany.

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http://dx.doi.org/10.1093/cvr/cvz054DOI Listing

Cardiomyocyte-specific Gq signaling and arrhythmias: novel insights from DREADD technology.

Cardiovasc Res 2019 Feb 22. Epub 2019 Feb 22.

European Laboratory for Non-Linear Spectroscopy (LENS), Sesto Fiorentino, Italy.

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http://dx.doi.org/10.1093/cvr/cvz052DOI Listing
February 2019

Cell-specific roles of p110β in myocardial ischemia.

Authors:
Alessandra Ghigo

Cardiovasc Res 2019 Feb 22. Epub 2019 Feb 22.

Department of Molecular Biotechnology and Health Sciences, University of Torino, Via Nizza 52, Torino, ITALY.

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http://dx.doi.org/10.1093/cvr/cvz051DOI Listing
February 2019