10,676 results match your criteria Cardiovascular research[Journal]


Focal TLR4 activation mediates disturbed flow-induced endothelial inflammation.

Cardiovasc Res 2019 Feb 20. Epub 2019 Feb 20.

Shenzhen Research Institute, Institute of Vascular Medicine, and Li Ka Shing Institute of Health Sciences, Chinese University of Hong Kong, Hong Kong, China.

Aims: Disturbed blood flow at arterial branches and curvatures modulates endothelial function and predisposes the region to endothelial inflammation and subsequent development of atherosclerotic lesions. Activation of the endothelial Toll-like receptors (TLRs), in particular TLR4, contributes to vascular inflammation. Therefore, we investigate whether TLR4 can sense disturbed flow to mediate the subsequent endothelial inflammation. 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/cvz046DOI Listing
February 2019
3 Reads

Identification of atheroprone shear stress responsive regulatory elements in endothelial cells.

Cardiovasc Res 2019 Feb 20. Epub 2019 Feb 20.

Institute of Anatomy and Vascular Biology, Westfälische Wilhelms-Universität Münster, Vesaliusweg 2-4, 48149 Münster, Germany.

Aim: Oscillatory shear stress (OSS) is an atheroprone hemodynamic force that occurs in areas of vessel irregularities and is implicated in the pathogenesis of atherosclerosis. Changes in signaling and transcriptional program in response to OSS have been vigorously studied, however, the underlying changes in the chromatin landscape controlling transcription remain to be elucidated. Here, we investigated the changes in the regulatory element (RE) landscape of endothelial cells under atheroprone OSS conditions in an in vitro model. Read More

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http://dx.doi.org/10.1093/cvr/cvz027DOI Listing
February 2019
1 Read

Macrophage-derived MMP-8 determines smooth muscle cell differentiation from adventitia stem/progenitor cells and promotes neointima hyperplasia.

Cardiovasc Res 2019 Feb 18. Epub 2019 Feb 18.

Department of Cardiology, the First Affiliated Hospital, School of Medicine, Zhejiang University, 79 Qingchun Road, Hangzhou, Zhejiang, China.

Objective: Emerging evidence has suggested that adventitia stem/progenitor cells (AdSPCs) migrate into the intima of arteries in response to injury, where they differentiate toward smooth muscle cells (SMCs) and participate in neointimal hyperplasia. We have previously identified matrix metalloproteinase-8 (MMP8) as a key player in atherogenesis. In this study, we aimed to investigate the functional roles of macrophage-derived MMP8 in AdSPC differentiation and injury-induced arterial remodelling. 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/cvz044DOI Listing
February 2019
1 Read

Increased ketone body oxidation provides additional energy for the failing heart without improving cardiac efficiency.

Cardiovasc Res 2019 Feb 18. Epub 2019 Feb 18.

Cardiovascular Research Centre Faculty of Medicine and Dentistry, University of Alberta, Edmonton, Alberta, Canada.

Aims: The failing heart is energy-starved and inefficient due to perturbations in energy metabolism. Although ketone oxidation has been shown recently to increase in the failing heart, it remains unknown whether this improves cardiac energy production or efficiency. We therefore assessed cardiac metabolism in failing hearts and determined whether increasing ketone oxidation improves cardiac energy production and efficiency. Read More

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http://dx.doi.org/10.1093/cvr/cvz045DOI Listing
February 2019

Stretching Single Titin Molecules from Failing Human Hearts Reveals Titin's Role in Blunting Cardiac Kinetic Reserve.

Cardiovasc Res 2019 Feb 18. Epub 2019 Feb 18.

Department of Physiology and Cell Biology, Cairo, Egypt.

Aims: Heart failure patients commonly experience symptoms primarily during elevated heart rates, as a result of physical activities or stress. A main determinant of diastolic passive tension, the elastic sarcomeric protein titin, has been shown to be associated with heart failure, with unresolved involvement regarding its role at different heart rates. To determine whether titin is playing a role in the heart rate (frequency-) dependent acceleration of relaxation (FDAR). Read More

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http://dx.doi.org/10.1093/cvr/cvz043DOI Listing
February 2019

Personalized Medicine in Cardio-Oncology: The Role of iPSC.

Cardiovasc Res 2019 Feb 15. Epub 2019 Feb 15.

Stanford Cardiovascular Institute, Stanford, California.

Treatment of cancer has evolved in the last decade with the introduction of new therapies. Despite these successes, the lingering cardiotoxic side-effects from chemotherapy remain a major cause of morbidity and mortality in cancer survivors. These effects can develop acutely during treatment, or even years later. Read More

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http://dx.doi.org/10.1093/cvr/cvz024DOI Listing
February 2019

Pediatric Cardio-Oncology: Epidemiology, Screening, Prevention, and Treatment.

Cardiovasc Res 2019 Feb 15. Epub 2019 Feb 15.

Department of Pediatrics, Seattle Children's Hospital, University of Washington, Seattle, WA, USA.

With five-year survival of children with cancer exceeding 80% in developed countries, premature cardiovascular disease is now a major cause of early morbidity and mortality. In addition to the acute and chronic cardiotoxic effects of anthracyclines, related chemotherapeutics, and radiation, a growing number of new molecular targeted agents may also have detrimental effects on the cardiovascular system. Survivors of childhood cancer also may have earlier development of conventional cardiovascular risk factors such as hypertension, dyslipidemia, and diabetes, which further increase their risk of serious cardiovascular disease. Read More

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http://dx.doi.org/10.1093/cvr/cvz031DOI Listing
February 2019
5.940 Impact Factor

Association of the coronary artery disease risk gene GUCY1A3 with ischaemic events after coronary intervention.

Cardiovasc Res 2019 Feb 14. Epub 2019 Feb 14.

Klinik für Herz- und Kreislauferkrankungen, Deutsches Herzzentrum München, Technische Universität München, Munich, Germany.

Aim: A common genetic variant at the GUCY1A3 coronary artery disease locus has been shown to influence platelet aggregation. The risk of ischaemic events including stent thrombosis varies with the efficacy of aspirin to inhibit platelet reactivity. This study sought to investigate whether homozygous GUCY1A3 (rs7692387) risk allele carriers display higher on-aspirin platelet reactivity and risk of ischaemic events early after coronary intervention. Read More

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http://dx.doi.org/10.1093/cvr/cvz015DOI Listing
February 2019
1 Read

Joint ESM-EVBO meetings: past, present and future.

Cardiovasc Res 2019 Feb 13. Epub 2019 Feb 13.

Department of Internal Medicine, CARIM, Maastricht University Medical Center, Maastricht, the Netherlands.

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http://dx.doi.org/10.1093/cvr/cvz041DOI Listing
February 2019

PBI-4050 Reduces Pulmonary Hypertension, Lung fibrosis and Right Ventricular Dysfunction in Heart Failure.

Cardiovasc Res 2019 Feb 7. Epub 2019 Feb 7.

Research Center of the Montreal Heart Institute.

Aims: Heart failure with reduced ejection fraction (HFrEF) causes lung remodelling with myofibroblasts proliferation and fibrosis leading to a restrictive lung syndrome with pulmonary hypertension (PH) and right ventricular (RV) dysfunction. PBI-4050 is a first-in-class anti-fibrotic, anti-inflammatory and anti-proliferative compound. The present study evaluated the therapeutic impact of PBI-4050 on PH in an HFrEF model. Read More

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http://dx.doi.org/10.1093/cvr/cvz034DOI Listing
February 2019
1 Read

Highlights of AHA Scientific Sessions 2018: a report from the Scientists of Tomorrow.

Cardiovasc Res 2019 Feb 6. Epub 2019 Feb 6.

Cardiovascular Cell Biology, Department of Cell and Chemical Biology, Postzone S-1-P, Leiden University Medical Center, RC Leiden, The Netherlands.

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http://dx.doi.org/10.1093/cvr/cvz005DOI Listing
February 2019

In-Vivo Ratiometric Optical Mapping Enables High-Resolution Cardiac Electrophysiology in Pig Models.

Cardiovasc Res 2019 Feb 7. Epub 2019 Feb 7.

Spanish National Cardiovascular Research Center, Carlos III (CNIC), Madrid, Spain.

Aims: Cardiac optical mapping is the gold standard for measuring complex electrophysiology in ex-vivo heart preparations. However, new methods for optical mapping in-vivo have been elusive. We aimed at developing and validating an experimental method for performing in-vivo cardiac optical mapping in pig models. 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/cvz039DOI Listing
February 2019
2 Reads

The curious case of dermal fibroblasts: cell identity loss may be a mechanism underlying cardiovascular aging.

Authors:
Ileana Badi

Cardiovasc Res 2019 Mar;115(3):e24-e25

Division of Cardiovascular Medicine, Radcliffe Department of Medicine, University of Oxford, John Radcliffe Hospital, Level 6 West Wing, Headley Way, Oxford, UK.

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http://dx.doi.org/10.1093/cvr/cvz012DOI Listing

Mesenchymal Stromal Cell-Derived Exosomes Attenuate Myocardial Ischemia-Reperfusion Injury through miR-182-Regulated Macrophage Polarization.

Cardiovasc Res 2019 Feb 8. Epub 2019 Feb 8.

Department of Cardiology, Drum Tower Hospital, Medical School of Nanjing University, Nanjing, China.

Aims: Mesenchymal stem cells (MSCs) gradually become attractive candidates for cardiac inflammation modulation, yet understanding of the mechanism remains elusive. Strikingly, recent studies indicated that exosomes secreted by MSCs might be a novel mechanism for the beneficial effect of MSCs transplantation after myocardial infarction. We therefore explored the role of MSC-derived exosomes (MSC-Exo) in the immunomodulation of macrophages after myocardial ischemia/reperfusion (I/R) and its implications in cardiac injury repair. Read More

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http://dx.doi.org/10.1093/cvr/cvz040DOI Listing
February 2019
1 Read

Microparticles from VEGF inhibitor-treated cancer patients mediate endothelial cell injury.

Cardiovasc Res 2019 Feb 11. Epub 2019 Feb 11.

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

Vascular endothelial growth factor pathway inhibitors (VEGFi), used as anti-angiogenic drugs to treat cancer are associated with cardiovascular toxicities through unknown molecular mechanisms. Endothelial cell-derived microparticles (ECMPs) are biomarkers of endothelial injury and are also functionally active since they influence downstream target cell signaling and function. We questioned whether microparticle (MP) status is altered in cancer patients treated with VEGFi and whether they influence endothelial cell function associated with vascular dysfunction. Read More

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http://dx.doi.org/10.1093/cvr/cvz021DOI Listing
February 2019
2 Reads

Scientists on the Spot: advances in cardiac surgery.

Cardiovasc Res 2019 Mar;115(3):e32-e33

San Raffaele University Hospital, via Olgettina 60, Milan, Italy.

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http://dx.doi.org/10.1093/cvr/cvz008DOI Listing

Cardioprotection in Cancer Therapy: Novel Insights with Anthracyclines.

Cardiovasc Res 2019 Feb 6. Epub 2019 Feb 6.

Harvard Medical School, Boston, Massachusetts.

Anthracyclines are a class of antineoplastic agents that remain critical to modern-day cancer treatment. However, their propensity to cause cardiotoxic effects limits their use and can cause increased morbidity and mortality among patients with cancer. Currently available methods to minimize the impact of anthracycline cardiotoxicity have not been widely successful. Read More

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http://dx.doi.org/10.1093/cvr/cvz023DOI Listing
February 2019

Vascular Cardio-Oncology: VEGF inhibitors and hypertension.

Cardiovasc Res 2019 Feb 6. Epub 2019 Feb 6.

Division of Vascular Medicine and Pharmacology, Department of Internal Medicine, Erasmus MC University Medical Center, Rotterdam, The Netherlands.

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http://dx.doi.org/10.1093/cvr/cvz022DOI Listing
February 2019
1 Read

Epidermal growth factor-like repeats of SCUBE1 derived from platelets are critical for thrombus formation.

Cardiovasc Res 2019 Feb 5. Epub 2019 Feb 5.

Institute of Biomedical Sciences, Academia Sinica, Taipei, Taiwan.

Aims: SCUBE1 (signal peptide-CUB-EGF domain-containing protein 1), expressed in endothelial cells (ECs) and platelets, exists in soluble or membrane forms. We previously showed that soluble SCUBE1 is a biomarker for platelet activation and also an active participant of thrombosis. However, whether the adhesive module of its EGF-like repeats is essential and the specific contribution of SCUBE1 synthesized in ECs or platelets to thrombosis in vivo remain unclear. Read More

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http://dx.doi.org/10.1093/cvr/cvz036DOI Listing
February 2019
1 Read

Coronary artery plaque characteristics and treatment with biologic therapy in severe psoriasis: results from a prospective observational study.

Cardiovasc Res 2019 Feb 5. Epub 2019 Feb 5.

Section of Inflammation and Cardiometabolic Disease, National Heart, Lung, and Blood Institute; National Institutes of Health, Bethesda, MD, USA.

Aims: The use of biologic therapy has increased over the past decade well beyond primary autoimmune diseases. Indeed, a recent trial using an anti-IL-1beta antibody reduced second myocardial infarction (MI) in those who have had MI. Psoriasis is a chronic inflammatory disease often treated with biologics when severe, is associated with increased risk of MI, in part driven by high-risk coronary plaque phenotypes by coronary computed tomography angiography (CCTA). Read More

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http://dx.doi.org/10.1093/cvr/cvz009DOI Listing
February 2019
1 Read

T Cell Checkpoint Regulators in the Heart.

Cardiovasc Res 2019 Feb 5. Epub 2019 Feb 5.

Department of Pathology Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts, USA.

T lymphocyte-mediated immune responses in the heart are potentially dangerous because they can interfere with the electromechanical function. Furthermore, the myocardium has limited regenerative capacity to repair damage caused by effector T cells. Myocardial T cell responses are normally suppressed by multiple mechanisms of central and peripheral tolerance. 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/cvz025DOI Listing
February 2019
4 Reads

Cardiac Sodium-Glucose Co-Transporter 1 (SGLT1) is a Novel Mediator of Ischemia/Reperfusion Injury.

Cardiovasc Res 2019 Feb 4. Epub 2019 Feb 4.

Division of Cardiovascular Medicine, Department of Internal Medicine, Carver College of Medicine and Abboud Cardiovascular Research Center, University of Iowa, Iowa City, IA.

Aims: We previously reported that sodium-dependent glucose cotransporter 1 (SGLT1) is highly expressed in cardiomyocytes, and is further upregulated in ischemia. This study aimed to determine the mechanisms by which SGLT1 contributes to ischemia/reperfusion (I/R) injury.

Methods And Results: Mice with cardiomyocyte-specific knockdown of SGLT1 (TGSGLT1-DOWN) and wildtype controls were studied. 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/cvz037DOI Listing
February 2019
4 Reads

Common risk factors for heart failure and cancer.

Cardiovasc Res 2019 Feb 4. Epub 2019 Feb 4.

University Medical Centre Groningen, University of Groningen, Department of Cardiology, AB 31, Hanzeplein 1, 9713GZ, Groningen, the Netherlands.

Cardiovascular (CV) disease and cancer are the leading causes of death.1,2 Over the last decades, it has been appreciated that both CV disease and cancer are more common in individuals in whom risk factors for disease development accumulate, and preventative measures have been extremely important in driving down the incidence of disease.3-6 In general, the field of epidemiology, risk reduction, and preventative trials is divided into health care professionals who have an interest in either CV disease or cancer. 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/cvz035DOI Listing
February 2019
3 Reads

Cardiovascular Toxicities Associated with Immune Checkpoint Inhibitors.

Cardiovasc Res 2019 02 2. Epub 2019 Feb 2.

Division of Cardiology, Cardio-Oncology Program, Vanderbilt University Medical Center, Nashville, TN, USA.

Cardiovascular toxicities associated with immune checkpoint inhibitors (ICIs) have been reported in case series but have been underappreciated due to difficulties in diagnosis and non-specific clinical manifestations. ICIs are antibodies that block negative regulators of the T cell immune response, including cytotoxic T-lymphocyte associated protein-4 (CTLA-4), programmed cell death protein-1 (PD-1), and PD-1 ligand (PD-L1). While ICIs have introduced a significant mortality benefit in several cancer types, the augmented immune response has led to a range of immune-related toxicities, including cardiovascular toxicity. Read More

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http://dx.doi.org/10.1093/cvr/cvz026DOI Listing
February 2019
1 Read
5.940 Impact Factor

Genome-wide identification of circulating-miRNA expression quantitative trait loci reveals the role of several miRNAs in the regulation of Cardiometabolic phenotypes.

Cardiovasc Res 2019 Jan 31. Epub 2019 Jan 31.

Ruddy Canadian Cardiovascular Genetics Centre, University of Ottawa Heart Institute, Ottawa, Canada.

Aims: To identify genetic variants that have a regulatory impact on circulating miRNAs and to connect genetic risk to blood traits/biomarkers through the circulating miRNAs.

Methods And Results: Leveraging miRNA-Seq data and the 1000 Genomes imputed genotypes, we carried out genome wide association analysis for SNPs that regulate the expression of circulating miRNAs in a sample of 710 unrelated subjects of European ancestry. Wherever possible, we used data from the Framingham and the Geuvadis studies to replicate our findings. 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/cvz030DOI Listing
January 2019
3 Reads

SERCA in heterogeneity of diastolic dysfunction in post-infarction heart failure with reduced ejection fraction.

Authors:
Masao Endoh

Cardiovasc Res 2019 Jan 31. Epub 2019 Jan 31.

Department of Pharmacology, Yamagata University School of Medicine, 2-2-2 Iida-nishi, Yamagata, Japan.

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http://dx.doi.org/10.1093/cvr/cvz017DOI Listing
January 2019

Perinatal iron deficiency and a high salt diet cause long-term kidney mitochondrial dysfunction and oxidative stress.

Cardiovasc Res 2019 Jan 31. Epub 2019 Jan 31.

Department of Pharmacology, University of Alberta.

Aims: Perinatal iron deficiency alters developmental trajectories of offspring, predisposing them to cardiovascular dysfunction in later life. The mechanisms underlying this long-term programming of renal function have not been defined. We hypothesized perinatal iron deficiency causes hypertension and alters kidney metabolic function and morphology in a sex-dependent manner in adult offspring. Read More

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http://dx.doi.org/10.1093/cvr/cvz029DOI Listing
January 2019
1 Read

Successful Renal Denervation Decreases the Platelet Activation Status in Hypertensive Patients.

Cardiovasc Res 2019 Feb 4. Epub 2019 Feb 4.

Atherothrombosis and Vascular Biology, Baker Heart and Diabetes Institute, Melbourne.

Aims: To determine whether renal denervation (RDN) in hypertensive patients affects the platelet activation status.

Methods And Results: We investigated the effect of RDN on the platelet activation status in 41 hypertensive patients undergoing RDN. Ambulatory blood pressure (BP), plasma sympathetic neurotransmitter Neuropeptide Y, and platelet activation markers were measured at baseline, at 3 months, and 6 months after RDN. Read More

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http://dx.doi.org/10.1093/cvr/cvz033DOI Listing
February 2019
4 Reads

Cardiac arrhythmia considerations of hormone cancer therapies.

Cardiovasc Res 2019 Jan 30. Epub 2019 Jan 30.

Department of Medicine and Clinical Pharmacology, Cardio-Oncology Program, Vanderbilt University Medical Center, Nashville, TN, USA.

Breast and prostate cancers are among the most prevalent cancers worldwide. Estradiol and progesterone are major drivers for breast cancer proliferation, as well as androgens for prostate cancer. Endocrine therapies are drugs that interfere with hormone-activated pathways to slow cancer progression. 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/cvz020DOI Listing
January 2019
10 Reads

Is IL-12 pro-inflammatory or anti-inflammatory? Depends on the blood pressure.

Cardiovasc Res 2019 Jan 30. Epub 2019 Jan 30.

Department of Medical Physiology, Texas A&M College of Medicine, College Station, TX USA.

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http://dx.doi.org/10.1093/cvr/cvz028DOI Listing
January 2019

Lansoprazole alleviates pressure overload-induced cardiac hypertrophy and heart failure in mice by blocking the activation of β-catenin.

Cardiovasc Res 2019 Jan 24. Epub 2019 Jan 24.

Department of Cardiology, State Key Laboratory of Organ Failure Research, Nanfang Hospital, Southern Medical University, Guangzhou, China.

Aims: Proton pump inhibitors (PPIs) are widely used in patients receiving percutaneous coronary intervention to prevent gastric bleeding, but whether PPIs are beneficial for the heart is controversial. Here we investigated the effects of lansoprazole on cardiac hypertrophy and heart failure, as well as the underlying mechanisms.

Methods And Results: Adult male C57 mice were subjected to transverse aortic constriction (TAC) or sham surgery and then were treated with lansoprazole or vehicle for 5 weeks. Read More

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http://dx.doi.org/10.1093/cvr/cvz016DOI Listing
January 2019
1 Read

Fibrin biofilm can be detected on intracoronary thrombi aspirated from patients with acute myocardial infarction.

Cardiovasc Res 2019 Jan 28. Epub 2019 Jan 28.

Institute of Cardiology, Jagiellonian University Medical College, Krakow, Poland and John Paul II Hospital, Krakow, Poland.

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http://dx.doi.org/10.1093/cvr/cvz019DOI Listing
January 2019

FoxO1 inhibits autophagosome-lysosome fusion leading to endothelial autophagic-apoptosis in diabetes.

Cardiovasc Res 2019 Jan 23. Epub 2019 Jan 23.

Department of Endocrinology, the First Affiliated Hospital with Nanjing Medical University, Nanjing, China.

Aims: Inadequate autophagy contributed to endothelial dysfunction in diabetic patients. We aimed to investigate the relationship between inadequate autophagy and endothelial cells (ECs) apoptosis in diabetes and its underlying mechanism.

Methods And Results: Aortic intima and ECs were isolated from diabetic patients. Read More

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http://dx.doi.org/10.1093/cvr/cvz014DOI Listing
January 2019

A current understanding of drug-induced QT prolongation and its implications for anticancer therapy.

Authors:
Dan M Roden

Cardiovasc Res 2019 Jan 23. Epub 2019 Jan 23.

Departments of Medicine, Pharmacology, and Biomedical Informatics, Vanderbilt University Medical Center, Nashville, TN.

The QT interval, a global index of ventricular repolarization, varies among individuals and is influenced by diverse physiologic and pathophysiologic stimuli such as gender, age, heart rate, electrolyte concentrations, concomitant cardiac disease, and other diseases such as diabetes. Many drugs produce a small but reproducible effect on QT interval but in rare instances this is exaggerated and marked QT prolongation can provoke the polymorphic ventricular tachycardia "torsades de pointes", which can cause syncope or sudden cardiac death. The generally accepted common mechanism whereby drugs prolong QT is block of a key repolarizing potassium current in heart, IKr, generated by expression of KCNH2, also known as HERG. Read More

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http://dx.doi.org/10.1093/cvr/cvz013DOI Listing
January 2019
2 Reads

hiPSCs in Cardio-Oncology: Deciphering the Genomics.

Cardiovasc Res 2019 Jan 24. Epub 2019 Jan 24.

Department of Pharmacology, Northwestern University Feinberg School of Medicine, Chicago, Illinois, USA.

The genomic predisposition to oncology-drug-induced cardiovascular toxicity has been postulated for many decades. Only recently has it become possible to experimentally validate this hypothesis via the use of patient-specific human induced pluripotent stem cells (hiPSCs) and suitably powered genome-wide association studies (GWAS). Identifying the individual single nucleotide polymorphisms (SNPs) responsible for the susceptibility to toxicity from a specific drug is a daunting task as this precludes the use of one of the most powerful tools in genomics: comparing phenotypes to close relatives, as these are highly unlikely to have been treated with the same drug. Read More

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http://dx.doi.org/10.1093/cvr/cvz018DOI Listing
January 2019

Scientists on the Spot: The future of genome editing in cardiovascular medicine.

Cardiovasc Res 2019 Feb;115(2):e20-e21

Cardiovascular Medicine and Genetics in the Perelman School of Medicine at the University of Pennsylvania, USA.

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http://dx.doi.org/10.1093/cvr/cvy302DOI Listing
February 2019

Leaders in Cardiovascular Research: Barbara Casadei.

Cardiovasc Res 2019 Feb;115(2):e17-e19

University of Oxford, Oxford, Oxon, UK.

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https://academic.oup.com/cardiovascres/article/115/2/e17/529
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http://dx.doi.org/10.1093/cvr/cvy303DOI Listing
February 2019
4 Reads

Challenges and advances of CRISPR-Cas9 genome editing in therapeutics.

Cardiovasc Res 2019 Feb;115(2):e12-e14

Division of Cardiology, Cardiovascular Institute, Department of Medicine, Perelman School of Medicine at the University of Pennsylvania, Philadelphia, PA, USA.

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http://dx.doi.org/10.1093/cvr/cvy300DOI Listing
February 2019

What have we learned about using aspirin for primary prevention from the ASCEND and ARRIVE trials?

Cardiovasc Res 2019 Feb;115(2):e15-e16

1st Cardiology Department, Hippokration Hospital, National and Kapodistrian University of Athens, 114 Vas. Sofias Ave, Athens, Greece.

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http://dx.doi.org/10.1093/cvr/cvy281DOI Listing
February 2019

Recent Cardiovascular Research highlights from the Americas.

Cardiovasc Res 2019 Feb;115(2):e22-e23

Department of Molecular Physiology and Biophysics, Vanderbilt University, Nashville, TN, USA.

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http://dx.doi.org/10.1093/cvr/cvy229DOI Listing
February 2019

ESC Working Group on Cellular Biology of the Heart: position paper for Cardiovascular Research: tissue engineering strategies combined with cell therapies for cardiac repair in ischaemic heart disease and heart failure.

Cardiovasc Res 2019 Mar;115(3):488-500

Department of Cardiology, Experimental Cardiology Laboratory, Regenerative Medicine Center, University Medical Center Utrecht, Utrecht University, Heidelberglaan 100, CX Utrecht, the Netherlands.

Morbidity and mortality from ischaemic heart disease (IHD) and heart failure (HF) remain significant in Europe and are increasing worldwide. Patients with IHD or HF might benefit from novel therapeutic strategies, such as cell-based therapies. We recently discussed the therapeutic potential of cell-based therapies and provided recommendations on how to improve the therapeutic translation of these novel strategies for effective cardiac regeneration and repair. 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/cvz010DOI Listing
March 2019
5 Reads

TNF-α Sets Area Postrema on Fire in Renovascular Hypertension.

Authors:
Jing Liu Jing Wu

Cardiovasc Res 2019 Jan 18. Epub 2019 Jan 18.

Department of Pharmacology, Carver College of Medicine, The University of Iowa, Iowa City, IA.

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http://dx.doi.org/10.1093/cvr/cvz011DOI Listing
January 2019
2 Reads
5.940 Impact Factor

Arrhythmogenetic Cardiomyopathy: In search of unifying genetic theory.

Cardiovasc Res 2019 Jan 12. Epub 2019 Jan 12.

Northwestern University - Feinberg School of Medicine.

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http://dx.doi.org/10.1093/cvr/cvy315DOI Listing
January 2019
1 Read

Delayed ischemic contracture onset by Empagliflozin associates with NHE-1 inhibition and is dependent on insulin in isolated mouse hearts.

Cardiovasc Res 2019 Jan 12. Epub 2019 Jan 12.

Amsterdam UMC, University of Amsterdam, Laboratory of Experimental Intensive Care and Anesthesiology, Anesthesiology, Amsterdam Cardiovascular Sciences, Amsterdam Infection & Immunity, Meibergdreef 9, Amsterdam, The Netherlands.

Aims: Sodium glucose cotransporter 2 (SGLT2) inhibitors have sodium-hydrogen exchanger (NHE) inhibition properties in isolated cardiomyocytes, but it is unknown whether these properties extend to the intact heart during ischemia-reperfusion (IR) conditions. NHE inhibitors as Cariporide delay time to onset of contracture (TOC) during ischemia and reduce IR injury. We hypothesized that, in the ex vivo heart, Empagliflozin (Empa) mimics Cariporide during IR by delaying TOC and reducing IR injury. Read More

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http://dx.doi.org/10.1093/cvr/cvz004DOI Listing
January 2019
1 Read
5.940 Impact Factor

The Intestine Responds to Heart Failure by Enhanced Mitochondrial Fusion through Glucagon-like Peptide-1 Signaling.

Cardiovasc Res 2019 Jan 10. Epub 2019 Jan 10.

Department of Cardiology, Gifu University Graduate School of Medicine, Gifu, Japan.

Aims: Glucagon-like peptide-1 (GLP-1) is a neuroendocrine hormone secreted by the intestine. Its receptor (GLP-1R) is expressed in various organs, including the heart. However, the dynamics and function of the GLP-1 signal in heart failure remains unclear. Read More

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http://dx.doi.org/10.1093/cvr/cvz002DOI Listing
January 2019
1 Read

Ponatinib-induced cardiotoxicity: delineating the signaling mechanisms and potential rescue strategies.

Cardiovasc Res 2019 Jan 10. Epub 2019 Jan 10.

Division of Cardiovascular Medicine, Vanderbilt University Medical Center, Nashville, TN, USA.

Aims: Tyrosine kinase inhibitors (TKIs) have revolutionized the treatment of chronic myelogenous leukemia (CML). However, cardiotoxicity of these agents remains a serious concern. The underlying mechanism of these adverse cardiac effects is largely unknown. Read More

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http://dx.doi.org/10.1093/cvr/cvz006DOI Listing
January 2019
2 Reads

Novel strategies to target proprotein convertase subtilisin kexin 9: beyond monoclonal antibodies.

Cardiovasc Res 2019 Mar;115(3):510-518

Center for the Study of Atherosclerosis, E. Bassini Hospital, Cinisello Balsamo, Milan, Italy.

Since the discovery of the role of proprotein convertase subtilisin kexin 9 (PCSK9) in the regulation of low-density lipoprotein cholesterol (LDL-C) in 2003, a paradigm shift in the treatment of hypercholesterolaemia has occurred. The PCSK9 secreted into the circulation is a major downregulator of the low-density lipoprotein receptor (LDLR) protein, as it chaperones it to endosomes/lysosomes for degradation. Humans with loss-of-function of PCSK9 exhibit exceedingly low levels of LDL-C and are protected from 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/cvz003DOI Listing
March 2019
11 Reads

Epigenetic Regulators of the Revascularization Response to Chronic Arterial Occlusion.

Cardiovasc Res 2019 Jan 10. Epub 2019 Jan 10.

Department of Biomedical Engineering, University of Virginia, Charlottesville, VA.

Peripheral arterial disease (PAD) is the leading cause of lower limb amputation and estimated to affect over 202 million people worldwide. PAD is caused by atherosclerotic lesions that occlude large arteries in the lower limbs, leading to insufficient blood perfusion of distal tissues. Given the severity of this clinical problem, there has been long-standing interest in both understanding how chronic arterial occlusions affect muscle tissue and vasculature and identifying therapeutic approaches capable of restoring tissue composition and vascular function to a healthy state. Read More

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http://dx.doi.org/10.1093/cvr/cvz001DOI Listing
January 2019
1 Read