Search our Database of Scientific Publications and Authors

I’m looking for a

    4060 results match your criteria Basic research in cardiology[Journal]

    1 OF 82

    The RISK pathway and beyond.
    Basic Res Cardiol 2017 Nov 15;113(1). Epub 2017 Nov 15.
    The Hatter Cardiovascular Institute, University College London, 67 Chenies Mews, London, WC1E 6HX, UK.
    Research on cardioprotection has attracted considerable attention during the past 30 years following the discovery of ischemic preconditioning with great advances being made in the field, particularly in the description of the molecular signalling behind this cardioprotective intervention. In a time when basic research is struggling to translate its findings into therapies in the clinical setting, this viewpoint has the intention of presenting to clinical and basic scientists how the reperfusion injury salvage kinase pathway has been described and dissected, as well as highlighting its relevance in cardioprotection. Read More

    Periostin in cardiovascular disease and development: a tale of two distinct roles.
    Basic Res Cardiol 2017 Nov 3;113(1). Epub 2017 Nov 3.
    Department of Physiology and Pathophysiology, Rady Faculty of Health Sciences, Max Rady College of Medicine, Institute of Cardiovascular Sciences, University of Manitoba, Winnipeg, Canada.
    Tissue development and homeostasis are dependent upon the concerted synthesis, maintenance, and degradation of extracellular matrix (ECM) molecules. Cardiac fibrosis is now recognized as a primary contributor to incidence of heart failure, particularly heart failure with preserved ejection fraction, wherein cardiac filling in diastole is compromised. Periostin is a cell-associated protein involved in cell fate determination, proliferation, tumorigenesis, and inflammatory responses. Read More

    Regenerating the human heart: direct reprogramming strategies and their current limitations.
    Basic Res Cardiol 2017 Oct 27;112(6):68. Epub 2017 Oct 27.
    Stem Cells for Tissue Engineering Lab, IRCCS Policlinico San Donato, Piazza Malan 2, San Donato Milanese, 20097, Milan, Italy.
    Cardiovascular diseases are the leading cause of death in the Western world. Unfortunately, current therapies are often only palliative, consequently essentially making heart transplantation necessary for many patients. However, several novel therapeutic approaches in the past two decades have yielded quite encouraging results. Read More

    Effect of long-term remote ischemic conditioning in patients with chronic ischemic heart failure.
    Basic Res Cardiol 2017 Oct 25;112(6):67. Epub 2017 Oct 25.
    Department of Cardiology, Aarhus University Hospital, Palle Juul-Jensens Boulevard 99, Aarhus N, 8200, Aarhus, Denmark.
    Remote ischemic conditioning (RIC) protects against acute ischemia-reperfusion injury and may also have beneficial effects in patients with stable cardiovascular disease. We investigated the effect of long-term RIC treatment in patients with chronic ischaemic heart failure (CIHF). In a parallel group study, 22 patients with compensated CIHF and 21 matched control subjects without heart failure or ischemic heart disease were evaluated by cardiac magnetic resonance imaging, cardiopulmonary exercise testing, skeletal muscle function testing, blood pressure measurement and blood sampling before and after 28 ± 4 days of once daily RIC treatment. Read More

    The role of PI3Kα isoform in cardioprotection.
    Basic Res Cardiol 2017 Oct 17;112(6):66. Epub 2017 Oct 17.
    The Hatter Cardiovascular Institute, University College London, 67 Chenies Mews, London, WC1E 6HX, UK.
    Ischemic preconditioning (IPC) limits myocardial infarct size through the activation of the PI3K-Akt signal cascade; however, little is known about the roles of individual PI3K isoforms in cardioprotection. We aimed, therefore, to elucidate the role of the PI3Kα isoform in cardioprotection Pharmacological PI3Kα inhibition was assessed in isolated-perfused mouse hearts subjected to ischemia/reperfusion injury (IRI), either during the IPC procedure or at reperfusion. PI3Kα inhibition abrogated the IPC-induced protective effect at reperfusion, but not when given only during the IPC protocol. Read More

    Regulation of myocardial oxygen delivery in response to graded reductions in hematocrit: role of K(+) channels.
    Basic Res Cardiol 2017 Sep 30;112(6):65. Epub 2017 Sep 30.
    Department of Cellular and Integrative Physiology, Indiana University School of Medicine, 635 Barnhill Drive, Indianapolis, IN, 46202, USA.
    This study was designed to identify mechanisms responsible for coronary vasodilation in response to progressive decreases in hematocrit. Isovolemic hemodilution was produced in open-chest, anesthetized swine via concurrent removal of 500 ml of arterial blood and the addition of 500 ml of 37 °C saline or synthetic plasma expander (Hespan, 6% hetastarch in 0.9% sodium chloride). Read More

    The impact of irreproducibility and competing protection from P2Y12 antagonists on the discovery of cardioprotective interventions.
    Basic Res Cardiol 2017 Sep 26;112(6):64. Epub 2017 Sep 26.
    Department of Physiology and Cell Biology, MSB 3050, University of South Alabama College of Medicine, Mobile, AL, 36688, USA.
    Scientists and clinicians have been concerned by the lack of a clinically suitable strategy for cardioprotection in patients with acute myocardial infarction despite decades of intensive pre-clinical investigations and a surprising number of clinical trials based on those observations which have uniformly been disappointing. However, it would be a mistake to abandon this search. Rather it would be useful to examine these past efforts and determine reasons for the multiple failures. Read More

    Oxidized low-density lipoprotein (oxLDL) affects load-free cell shortening of cardiomyocytes in a proprotein convertase subtilisin/kexin 9 (PCSK9)-dependent way.
    Basic Res Cardiol 2017 Sep 14;112(6):63. Epub 2017 Sep 14.
    Institute of Physiology, Justus-Liebig-University Giessen, Aulweg 129, 35392, Giessen, Germany.
    Recent studies have documented that oxidized low-density lipoprotein cholesterol (oxLDL) levels directly impact myocardial structure and function. However, the molecular mechanisms by which oxLDL affects cardiac myocytes are not well established. We addressed the question whether oxLDL modifies load-free cell shortening, a standardized readout of cardiac cellular function, and investigated whether proprotein convertase subtilisin/kexin-9 (PCSK9) is involved on oxLDL-dependent processes. Read More

    Dual inhibition of cathepsin G and chymase reduces myocyte death and improves cardiac remodeling after myocardial ischemia reperfusion injury.
    Basic Res Cardiol 2017 Sep 14;112(6):62. Epub 2017 Sep 14.
    Cardiovascular Research Center, Lewis Katz School of Medicine, Temple University, MERB 1045, 3500 N. Broad Street, Philadelphia, PA, 19140, USA.
    Early reperfusion of ischemic cardiac tissue increases inflammatory cell infiltration which contributes to cardiomyocyte death and loss of cardiac function, referred to as ischemia/reperfusion (IR) injury. Neutrophil- and mast cell-derived proteases, cathepsin G (Cat.G) and chymase, are released early after IR, but their function is complicated by potentially redundant actions and targets. Read More

    Influence of increased heart rate and aortic pressure on resting indices of functional coronary stenosis severity.
    Basic Res Cardiol 2017 Sep 13;112(6):61. Epub 2017 Sep 13.
    Department of Biomedical Engineering and Physics, Academic Medical Center, University of Amsterdam, PO Box 22660, 1100 DD, Amsterdam, The Netherlands.
    Baseline assessment of functional stenosis severity has been proposed as a practical alternative to hyperemic indices. However, intact autoregulation mechanisms may affect intracoronary hemodynamics. The aim of this study was to investigate the effect of changes in aortic pressure (Pa) and heart rate (HR) on baseline coronary hemodynamics and functional stenosis assessment. Read More

    Disruption of adenylyl cyclase type 5 mimics exercise training.
    Basic Res Cardiol 2017 Sep 8;112(6):59. Epub 2017 Sep 8.
    Department of Cell Biology and Molecular Medicine, Cardiovascular Research Institute, New Jersey Medical School, Rutgers University, 185 South Orange Avenue, MSB G609, Newark, NJ, 07103, USA.
    Exercise training is key to healthful longevity. Since exercise training compliance is difficult, it would be useful to have a therapeutic substitute that mimicked exercise training. We compared the effects of exercise training in wild-type (WT) littermates with adenylyl cyclase type 5 knock out (AC5 KO) mice, a model of enhanced exercise performance. Read More

    MicroRNA-143 promotes cardiac ischemia-mediated mitochondrial impairment by the inhibition of protein kinase Cepsilon.
    Basic Res Cardiol 2017 Sep 8;112(6):60. Epub 2017 Sep 8.
    Department of Pharmacology (State-Province Key Laboratories of Biomedicine-Pharmaceutics of China, Key Laboratory of Cardiovascular Medicine Research, Ministry of Education), College of Pharmacy, Harbin Medical University, Harbin, China.
    The cardioprotection of protein kinase Cepsilon (PKCε) against myocardial infarction (MI) mediated by its anti-apoptotic property and underlying mechanism of targeted regulation by microRNA (miRNA) are not established. MI-induced injury, PKCε expression, and targeted regulation of miRNA-143 (miR-143) to PKCε have been evaluated using animal MI and cellular hypoxic models conjugated with series of state-of-art molecular techniques. The results demonstrated that PKCε significantly downregulated along with increased infarcted area and apoptotic and necrotic damage in MI model, and the targeted relationship and potential binding profile were established between miR-143 and PKCε. Read More

    Transforming growth factor-β-mediated CD44/STAT3 signaling contributes to the development of atrial fibrosis and fibrillation.
    Basic Res Cardiol 2017 Sep 4;112(5):58. Epub 2017 Sep 4.
    Cardiovascular Division, Chang-Gung Memorial Hospital, Chang-Gung University College of Medicine, Fu-Shin Road No. 5, Kwei-Shan, Taoyuan, 333, Taiwan.
    Atrial fibrillation (AF) is associated with atrial fibrosis. Inhibition of atrial fibrosis might be a plausible approach for AF prevention and therapy. This study is designed to evaluate the potential role of CD44, a membrane receptor known to regulate fibrosis, and its related signaling in the pathogenesis of atrial fibrosis and AF. Read More

    Methylglyoxal-derived advanced glycation end products contribute to negative cardiac remodeling and dysfunction post-myocardial infarction.
    Basic Res Cardiol 2017 Sep 1;112(5):57. Epub 2017 Sep 1.
    Division of Cardiac Surgery, University of Ottawa Heart Institute, 40 Ruskin Street, Ottawa, K1Y4W7, Canada.
    Advanced glycation end-products (AGEs) have been associated with poorer outcomes after myocardial infarction (MI), and linked with heart failure. Methylglyoxal (MG) is considered the most important AGE precursor, but its role in MI is unknown. In this study, we investigated the involvement of MG-derived AGEs (MG-AGEs) in MI using transgenic mice that over-express the MG-metabolizing enzyme glyoxalase-1 (GLO1). Read More

    Cardiac optogenetics: using light to monitor cardiac physiology.
    Basic Res Cardiol 2017 Aug 31;112(5):56. Epub 2017 Aug 31.
    Department of Medical Physiology, University Medical Center Utrecht, Yalelaan 50, 3584CM, Utrecht, The Netherlands.
    Our current understanding of cardiac excitation and its coupling to contraction is largely based on ex vivo studies utilising fluorescent organic dyes to assess cardiac action potentials and signal transduction. Recent advances in optogenetic sensors open exciting new possibilities for cardiac research and allow us to answer research questions that cannot be addressed using the classic organic dyes. Especially thrilling is the possibility to use optogenetic sensors to record parameters of cardiac excitation and contraction in vivo. Read More

    Cardiomyocyte dimethylarginine dimethylaminohydrolase-1 (DDAH1) plays an important role in attenuating ventricular hypertrophy and dysfunction.
    Basic Res Cardiol 2017 Aug 17;112(5):55. Epub 2017 Aug 17.
    Cardiovascular Division, University of Minnesota Medical School, Minneapolis, USA.
    Asymmetric dimethylarginine (ADMA) is an endogenous inhibitor of nitric oxide synthases that limits nitric oxide bioavailability. Dimethylarginine dimethylaminohydrolase-1 (DDAH1) exerts a critical role for ADMA degradation and plays an important role in NO signaling. In the heart, DDAH1 is observed in endothelial cells and in the sarcolemma of cardiomyocytes. Read More

    Long-term spironolactone treatment reduces coronary TRPC expression, vasoconstriction, and atherosclerosis in metabolic syndrome pigs.
    Basic Res Cardiol 2017 Sep 29;112(5):54. Epub 2017 Jul 29.
    Department of Cellular and Integrative Physiology, Indiana University School of Medicine, Indianapolis, 635 Barnhill Dr., MS360A, Indianapolis, IN, 46202, USA.
    Coronary transient receptor potential canonical (TRPC) channel expression is elevated in metabolic syndrome (MetS). However, differential contribution of TRPCs to coronary pathology in MetS is not fully elucidated. We investigated the roles of TRPC1 and TRPC6 isoforms in coronary arteries of MetS pigs and determined whether long-term treatment with a mineralocorticoid receptor inhibitor, spironolactone, attenuates coronary TRPC expression and associated dysfunctions. Read More

    Cardioprotection by the transfer of coronary effluent from ischaemic preconditioned rat hearts: identification of cardioprotective humoral factors.
    Basic Res Cardiol 2017 Sep 10;112(5):52. Epub 2017 Jul 10.
    Laboratory of Cardiac Electrophysiology Antonio Paes de Carvalho, Institute of Biophysics Carlos Chagas Filho, CCS, Federal University of Rio de Janeiro (UFRJ), Av. Carlos Chagas Filho, 373, CCS Bloco G, Ilha do Fundao, 21941-902, Rio de Janeiro, RJ, Brazil.
    Ischaemic preconditioning (IPC) provides myocardial resistance to ischaemia/reperfusion (I/R) injuries. The protection afforded by IPC is not limited to the target tissue but extends to remote tissues, suggesting a mechanism mediated by humoral factors. The aim of the present study was to identify the humoral factors that are responsible for the cardioprotection induced by the coronary effluent transferred from IPC to naïve hearts. Read More

    Animal models of arrhythmogenic right ventricular cardiomyopathy: what have we learned and where do we go? Insight for therapeutics.
    Basic Res Cardiol 2017 Sep 7;112(5):50. Epub 2017 Jul 7.
    CIBER Cardiovascular Diseases (CIBERCV), Madrid, Spain.
    Arrhythmogenic right ventricular cardiomyopathy (ARVC) is a rare genetically-determined cardiac heart muscle disorder characterized by fibro-fatty replacement of the myocardium that results in heart failure and sudden cardiac death (SCD), predominantly in young males. The disease is often caused by mutations in genes encoding proteins of the desmosomal complex, with a significant minority caused by mutations in non-desmosomal proteins. Existing treatment options are based on SCD prevention with the implantable cardioverter defibrillator, antiarrhythmic drugs, and anti-heart failure medication. Read More

    Exogenous GDF11 induces cardiac and skeletal muscle dysfunction and wasting.
    Basic Res Cardiol 2017 Jul 24;112(4):48. Epub 2017 Jun 24.
    Department of Surgery, Indiana University School of Medicine, 545 Barnhill Drive, Emerson 511, Indianapolis, IN, 46202, USA.
    Growth differentiation factor 11 (GDF11), a TGF-beta superfamily member, is highly homologous to myostatin and essential for embryonic patterning and organogenesis. Reports of GDF11 effects on adult tissues are conflicting, with some describing anti-aging and pro-regenerative activities on the heart and skeletal muscle while others opposite or no effects. Herein, we sought to determine the in vivo cardiac and skeletal muscle effects of excess GDF11. Read More

    The crucial role of activin A/ALK4 pathway in the pathogenesis of Ang-II-induced atrial fibrosis and vulnerability to atrial fibrillation.
    Basic Res Cardiol 2017 Jul 21;112(4):47. Epub 2017 Jun 21.
    Department of Cardiology, Xinhua Hospital, School of Medicine, Shanghai Jiao Tong University, 1665 Kongjiang Road, Shanghai, 200092, China.
    Atrial fibrosis, the hallmark of structural remodeling associated with atrial fibrillation (AF), is characterized by abnormal proliferation of atrial fibroblasts and excessive deposition of extracellular matrix. Transforming growth factor-β1 (TGF-β1)/activin receptor-like kinase 5 (ALK5)/Smad2/3/4 pathway has been reported to be involved in the process. Recent studies have implicated both activin A and its specific downstream component activin receptor-like kinase 4 (ALK4) in stimulating fibrosis in non-cardiac organs. Read More

    Deleterious acute and chronic effects of bradycardic right ventricular apex pacing: consequences for arrhythmic outcome.
    Basic Res Cardiol 2017 Jul 17;112(4):46. Epub 2017 Jun 17.
    Department of Medical Physiology, University Medical Center Utrecht, Yalelaan 50, 3584 CM, Utrecht, The Netherlands.
    In the chronic complete atrioventricular (AV) block dog (CAVB) model, both bradycardia and altered ventricular activation due to the uncontrolled idioventricular rhythm contribute to ventricular remodeling and the enhanced susceptibility to Torsade de Pointes (TdP) arrhythmias. We investigated the effect of permanent bradycardic right ventricular apex (RVA) pacing on mechanical and electrical remodeling and TdP. In 23 anesthetized dogs, serial experiments were performed at sinus rhythm (SR), acutely after AV block (AAVB) and 3 weeks of remodeling CAVB at a fixed pacing rate of 60/min. Read More

    Reduction of SR Ca(2+) leak and arrhythmogenic cellular correlates by SMP-114, a novel CaMKII inhibitor with oral bioavailability.
    Basic Res Cardiol 2017 Jul 13;112(4):45. Epub 2017 Jun 13.
    Klinik für Innere Medizin II, Universitätsklinikum Regensburg, Franz-Josef-Strauß-Allee 11, 93053, Regensburg, Germany.
    Sarcoplasmic reticulum (SR) Ca(2+) leak induced by Ca(2+)/calmodulin-dependent protein kinase II (CaMKII) is centrally involved in atrial and ventricular arrhythmogenesis as well as heart failure remodeling. Consequently, treating SR Ca(2+) leak has been proposed as a novel therapeutic paradigm, but compounds for use in humans are lacking. SMP-114 ("Rimacalib") is a novel, orally available CaMKII inhibitor developed for human use that has already entered clinical phase II trials to treat rheumatoid arthritis. Read More

    The role of spatial organization of Ca(2+) release sites in the generation of arrhythmogenic diastolic Ca(2+) release in myocytes from failing hearts.
    Basic Res Cardiol 2017 Jul 13;112(4):44. Epub 2017 Jun 13.
    Department of Physiology and Cell Biology, The Ohio State University, Columbus, OH, 43210, USA.
    In heart failure (HF), dysregulated cardiac ryanodine receptors (RyR2) contribute to the generation of diastolic Ca(2+) waves (DCWs), thereby predisposing adrenergically stressed failing hearts to life-threatening arrhythmias. However, the specific cellular, subcellular, and molecular defects that account for cardiac arrhythmia in HF remain to be elucidated. Patch-clamp techniques and confocal Ca(2+) imaging were applied to study spatially defined Ca(2+) handling in ventricular myocytes isolated from normal (control) and failing canine hearts. Read More

    Differential regulation of protein phosphatase 1 (PP1) isoforms in human heart failure and atrial fibrillation.
    Basic Res Cardiol 2017 Jul 9;112(4):43. Epub 2017 Jun 9.
    Department of Pharmacology and Toxicology, Medical Faculty, Technische Universität Dresden, Fetscherstraße 74, Dresden, 01307, Germany.
    Protein phosphatase 1 (PP1) is a key regulator of important cardiac signaling pathways. Dysregulation of PP1 has been heavily implicated in cardiac dysfunctions. Accordingly, pharmacological targeting of PP1 activity is considered for therapeutic intervention in human cardiomyopathies. Read More

    Sema3A promotes the resolution of cardiac inflammation after myocardial infarction.
    Basic Res Cardiol 2017 Jul 24;112(4):42. Epub 2017 May 24.
    Cardiovascular Research Institute Maastricht, Universiteitssingel 50, 6229 ER, Maastricht, The Netherlands.
    Optimal healing after myocardial infarction requires not only the induction of inflammation, but also its timely resolution. In patients, 30 days post myocardial infarction, circulating monocytes have increased expression of Semaphorin3A (Sema3A) as compared to directly after admission. This increased expression coincides with increased expression of Cx3CR1-a marker of non-classical monocytes that are important for immune resolution hence proper wound healing. Read More

    Alignment of inducible vascular progenitor cells on a micro-bundle scaffold improves cardiac repair following myocardial infarction.
    Basic Res Cardiol 2017 Jul 24;112(4):41. Epub 2017 May 24.
    Department of Integrative Medical Sciences, Northeast Ohio Medical University, 4209 State Route 44, Rootstown, OH, 44272, USA.
    Ischemic heart disease is still the leading cause of death even with the advancement of pharmaceutical therapies and surgical procedures. Early vascularization in the ischemic heart is critical for a better outcome. Although stem cell therapy has great potential for cardiovascular regeneration, the ideal cell type and delivery method of cells have not been resolved. Read More

    Splenic Ly6C(hi) monocytes contribute to adverse late post-ischemic left ventricular remodeling in heme oxygenase-1 deficient mice.
    Basic Res Cardiol 2017 Jul 22;112(4):39. Epub 2017 May 22.
    Department of Medical Biotechnology, Faculty of Biochemistry, Biophysics and Biotechnology, Jagiellonian University, Gronostajowa 7, 30-387, Krakow, Poland.
    Heme oxygenase-1 (Hmox1) is a stress-inducible protein crucial in heme catabolism. The end products of its enzymatic activity possess anti-oxidative, anti-apoptotic and anti-inflammatory properties. Cardioprotective effects of Hmox1 were demonstrated in experimental models of myocardial infarction (MI). Read More

    Exercise-induced circulating extracellular vesicles protect against cardiac ischemia-reperfusion injury.
    Basic Res Cardiol 2017 Jul 22;112(4):38. Epub 2017 May 22.
    Cardiac Regeneration and Ageing Lab, School of Life Science, Shanghai University, 333 Nan Chen Road, Shanghai, 200444, China.
    Extracellular vesicles (EVs) serve an important function as mediators of intercellular communication. Exercise is protective for the heart, although the signaling mechanisms that mediate this cardioprotection have not been fully elucidated. Here using nano-flow cytometry, we found a rapid increase in plasma EVs in human subjects undergoing exercise stress testing. Read More

    Expression and regulation of type 2A protein phosphatases and alpha4 signalling in cardiac health and hypertrophy.
    Basic Res Cardiol 2017 Jul 19;112(4):37. Epub 2017 May 19.
    School of Life Sciences, Pharmacy and Chemistry, Faculty of Science Engineering and Computing, Kingston University, Penrhyn Road, Kingston-upon-Thames, Surrey, KT1 2EE, UK.
    Cardiac physiology and hypertrophy are regulated by the phosphorylation status of many proteins, which is partly controlled by a poorly defined type 2A protein phosphatase-alpha4 intracellular signalling axis. Quantitative PCR analysis revealed that mRNA levels of the type 2A catalytic subunits were differentially expressed in H9c2 cardiomyocytes (PP2ACβ > PP2ACα > PP4C > PP6C), NRVM (PP2ACβ > PP2ACα = PP4C = PP6C), and adult rat ventricular myocytes (PP2ACα > PP2ACβ > PP6C > PP4C). Western analysis confirmed that all type 2A catalytic subunits were expressed in H9c2 cardiomyocytes; however, PP4C protein was absent in adult myocytes and only detectable following 26S proteasome inhibition. Read More

    Impairment of pH gradient and membrane potential mediates redox dysfunction in the mitochondria of the post-ischemic heart.
    Basic Res Cardiol 2017 Jul 16;112(4):36. Epub 2017 May 16.
    Department of Integrative Medical Sciences, College of Medicine, Northeast Ohio Medical University, 4209 State Route 44, PO Box 95, Rootstown, OH, 44272, USA.
    The mitochondrial electrochemical gradient (Δp), which comprises the pH gradient (ΔpH) and the membrane potential (ΔΨ), is crucial in controlling energy transduction. During myocardial ischemia and reperfusion (IR), mitochondrial dysfunction mediates superoxide ((·)O2(-)) and H2O2 overproduction leading to oxidative injury. However, the role of ΔpH and ΔΨ in post-ischemic injury is not fully established. Read More

    Fast therapeutic hypothermia prevents post-cardiac arrest syndrome through cyclophilin D-mediated mitochondrial permeability transition inhibition.
    Basic Res Cardiol 2017 Jul 10;112(4):35. Epub 2017 May 10.
    Hospices Civils de Lyon, Hôpital Edouard Herriot, Service de Réanimation Médicale, 5 Place d'Arsonval, 69437, Lyon Cedex 03, France.
    The opening of the mitochondrial permeability transition pore (PTP), which is regulated by the matrix protein cyclophilin D (CypD), plays a key role in the pathophysiology of post-cardiac arrest (CA) syndrome. We hypothesized that therapeutic hypothermia could prevent post-CA syndrome through a CypD-mediated PTP inhibition in both heart and brain. In addition, we investigated whether specific pharmacological PTP inhibition would confer additive protection to cooling. Read More

    Dissecting the role of myeloid and mesenchymal fibroblasts in age-dependent cardiac fibrosis.
    Basic Res Cardiol 2017 Jul 6;112(4):34. Epub 2017 May 6.
    Division of Cardiovascular Sciences and the DeBakey Heart Center, Department of Medicine, Baylor College of Medicine, One Baylor Plaza, M.S. BCM620, Houston, TX, 77030, USA.
    Aging is associated with increased cardiac interstitial fibrosis and diastolic dysfunction. Our previous study has shown that mesenchymal fibroblasts in the C57BL/6J (B6J) aging mouse heart acquire an inflammatory phenotype and produce higher levels of chemokines. Monocyte chemoattractant protein-1 (MCP-1) secreted by these aged fibroblasts promotes leukocyte uptake into the heart. Read More

    IL-10 improves cardiac remodeling after myocardial infarction by stimulating M2 macrophage polarization and fibroblast activation.
    Basic Res Cardiol 2017 May 24;112(3):33. Epub 2017 Apr 24.
    Department of Physiology and Biophysics, Mississippi Center for Heart Research, University of Mississippi Medical Center, 2500 North State St., Jackson, MS, 39216-4505, USA.
    Inflammation resolution is important for scar formation following myocardial infarction (MI) and requires the coordinated actions of macrophages and fibroblasts. In this study, we hypothesized that exogenous interleukin-10 (IL-10), an anti-inflammatory cytokine, promotes post-MI repair through actions on these cardiac cell types. To test this hypothesis, C57BL/6J mice (male, 3- to 6-month old, n = 24/group) were treated with saline or IL-10 (50 μg/kg/day) by osmotic mini-pump infusion starting at day (d) 1 post-MI and sacrificed at d7 post-MI. Read More

    Physiological and therapeutic regulation of PCSK9 activity in cardiovascular disease.
    Basic Res Cardiol 2017 May 24;112(3):32. Epub 2017 Apr 24.
    Department of Physiology, Justus-Liebig-University, Aulweg 129, 35392, Giessen, Germany.
    Ischemic heart disease is the main cause of death worldwide and is accelerated by increased levels of low-density lipoprotein cholesterol (LDL-C). Proprotein convertase subtilisin/kexin type 9 (PCSK9) is a potent circulating regulator of LDL-C through its ability to induce degradation of the LDL receptor (LDLR) in the lysosome of hepatocytes. Only in the last few years, a number of breakthroughs in the understanding of PCSK9 biology have been reported illustrating how PCSK9 activity is tightly regulated at several levels by factors influencing its transcription, secretion, or by extracellular inactivation and clearance. Read More

    Insufficient activation of Akt upon reperfusion because of its novel modification by reduced PP2A-B55α contributes to enlargement of infarct size by chronic kidney disease.
    Basic Res Cardiol 2017 May 18;112(3):31. Epub 2017 Apr 18.
    Department of Cardiovascular, Renal and Metabolic Medicine, Sapporo Medical University, South-1 West-16, Chuo-ku, Sapporo, 060-8543, Japan.
    Chronic kidney disease (CKD) increases myocardial infarct size by an unknown mechanism. Here we examined the hypothesis that impairment of protective PI3K-PDK1-Akt and/or mTORC-Akt signaling upon reperfusion contributes to CKD-induced enlargement of infarct size. CKD was induced in rats by 5/6 nephrectomy (SNx group) 4 weeks before myocardial infarction experiments, and sham-operated rats served as controls (Sham group). Read More

    Aquaporin 1 controls the functional phenotype of pulmonary smooth muscle cells in hypoxia-induced pulmonary hypertension.
    Basic Res Cardiol 2017 May 13;112(3):30. Epub 2017 Apr 13.
    Division of Pulmonology, University Hospital Zurich, University of Zurich, Zurich, Switzerland.
    Vascular remodelling in hypoxia-induced pulmonary hypertension (PH) is driven by excessive proliferation and migration of endothelial and smooth muscle cells. The expression of aquaporin 1 (AQP1), an integral membrane water channel protein involved in the control of these processes, is tightly regulated by oxygen levels. The role of AQP1 in the pathogenesis of PH, however, has not been directly addressed so far. Read More

    Sex-difference in expression and function of beta-adrenoceptors in macrovessels: role of the endothelium.
    Basic Res Cardiol 2017 May 7;112(3):29. Epub 2017 Apr 7.
    Department of Physiology, Medical Faculty Carl Gustav Carus, Technische Universität Dresden, Fetscherstr. 74, 01307, Dresden, Germany.
    Estrogen modulates adrenergic reactivity of macrovessels, resulting in weaker α-adrenergic vasoconstriction in females than males. However, the mechanisms governing this important sex-specific difference are not well understood. We hypothesized that vessels of females express more dilatory β-adrenoceptors, which counteract constrictive effects of α-adrenoceptors. Read More

    Intermittent pacing therapy favorably modulates infarct remodeling.
    Basic Res Cardiol 2017 May 6;112(3):28. Epub 2017 Apr 6.
    Department of Cardiology, Ee-2351, Erasmus MC, University Medical Center Rotterdam, PO Box 2040, 3000 CA, Rotterdam, The Netherlands.
    Despite early revascularization, remodeling and dysfunction of the left ventricle (LV) after acute myocardial infarction (AMI) remain important therapeutic targets. Intermittent pacing therapy (IPT) of the LV can limit infarct size, when applied during early reperfusion. However, the effects of IPT on post-AMI LV remodeling and infarct healing are unknown. Read More

    Mitochondrial Cx43 hemichannels contribute to mitochondrial calcium entry and cell death in the heart.
    Basic Res Cardiol 2017 May 31;112(3):27. Epub 2017 Mar 31.
    Physiology Group, Department of Basic Medical Sciences, Faculty of Medicine and Health Sciences, Ghent University, De Pintelaan 185 (Block B, Rm 031), 9000, Ghent, Belgium.
    Mitochondrial connexin 43 (Cx43) plays a key role in cardiac cytoprotection caused by repeated exposure to short periods of non-lethal ischemia/reperfusion, a condition known as ischemic preconditioning. Cx43 also forms calcium (Ca(2+))-permeable hemichannels that may potentially lead to mitochondrial Ca(2+) overload and cell death. Here, we studied the role of Cx43 in facilitating mitochondrial Ca(2+) entry and investigated its downstream consequences. Read More

    Effect of paroxetine on left ventricular remodeling in an in vivo rat model of myocardial infarction.
    Basic Res Cardiol 2017 May 27;112(3):26. Epub 2017 Mar 27.
    Department of Cardiology, Aarhus University Hospital, Skejby, Palle Juul-Jensens Boulevard 99, 8200, Aarhus, Denmark.
    Left ventricular (LV) remodeling following a myocardial infarction (MI) involves formation of reactive oxygen species (ROS). Paroxetine, a selective serotonin reuptake inhibitor, has an antioxidant effect in the vascular wall. We investigated whether paroxetine reduces myocardial ROS formation and LV remodeling following a MI. Read More

    Role of bone marrow-derived CD11c(+) dendritic cells in systolic overload-induced left ventricular inflammation, fibrosis and hypertrophy.
    Basic Res Cardiol 2017 May 27;112(3):25. Epub 2017 Mar 27.
    Cardiovascular Division and Lillehei Heart Institute, University of Minnesota Medical School, Minneapolis, MN, 55455, USA.
    Inflammatory responses play an important role in the development of left ventricular (LV) hypertrophy and dysfunction. Recent studies demonstrated that increased T-cell infiltration and T-cell activation contribute to LV hypertrophy and dysfunction. Dendritic cells (DCs) are professional antigen-presenting cells that orchestrate immune responses, especially by modulating T-cell function. Read More

    Cavin-1 deficiency modifies myocardial and coronary function, stretch responses and ischaemic tolerance: roles of NOS over-activity.
    Basic Res Cardiol 2017 May 25;112(3):24. Epub 2017 Mar 25.
    School of Medical Science, Griffith University, Southport, QLD, 4217, Australia.
    Caveolae and associated cavin and caveolins may govern myocardial function, together with responses to mechanical and ischaemic stresses. Abnormalities in these proteins are also implicated in different cardiovascular disorders. However, specific roles of the cavin-1 protein in cardiac and coronary responses to mechanical/metabolic perturbation remain unclear. Read More

    Cardiomyocyte Ogt limits ventricular dysfunction in mice following pressure overload without affecting hypertrophy.
    Basic Res Cardiol 2017 May 15;112(3):23. Epub 2017 Mar 15.
    Division of Cardiovascular Medicine, Department of Medicine, Institute of Molecular Cardiology, Diabetes and Obesity Center, University of Louisville, 580 South Preston Street, Louisville, KY, 40202, USA.
    The myocardial response to pressure overload involves coordination of multiple transcriptional, posttranscriptional, and metabolic cues. The previous studies show that one such metabolic cue, O-GlcNAc, is elevated in the pressure-overloaded heart, and the increase in O-GlcNAcylation is required for cardiomyocyte hypertrophy in vitro. Yet, it is not clear whether and how O-GlcNAcylation participates in the hypertrophic response in vivo. Read More

    SUV39H1 mediated SIRT1 trans-repression contributes to cardiac ischemia-reperfusion injury.
    Basic Res Cardiol 2017 May 8;112(3):22. Epub 2017 Mar 8.
    Key Laboratory of Cardiovascular Disease and Molecular Intervention, Department of Pathophysiology, Nanjing Medical University, 140 Hanzhong Rd, Nanjing, 210029, Jiangsu, China.
    Ischemic reperfusion (I/R) contributes to deleterious cardiac remodeling and heart failure. The deacetylase SIRT1 has been shown to protect the heart from I/R injury. We examined the mechanism whereby I/R injury represses SIRT1 transcription in the myocardium. Read More

    Vasopressors induce passive pulmonary hypertension by blood redistribution from systemic to pulmonary circulation.
    Basic Res Cardiol 2017 May 3;112(3):21. Epub 2017 Mar 3.
    Department of Anesthesiology and Translational Neuroscience Center, West China Hospital, Sichuan University, Chengdu, 610041, Sichuan, China.
    Vasopressors are widely used in resuscitation, ventricular failure, and sepsis, and often induce pulmonary hypertension with undefined mechanisms. We hypothesize that vasopressor-induced pulmonary hypertension is caused by increased pulmonary blood volume and tested this hypothesis in dogs under general anesthesia. In normal hearts (model 1), phenylephrine (2. Read More

    1 OF 82