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Basic Research in Cardiology

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https://www.readbyqxmd.com/read/28695353/cardioprotection-by-the-transfer-of-coronary-effluent-from-ischaemic-preconditioned-rat-hearts-identification-of-cardioprotective-humoral-factors
#1
Leonardo Maciel, Dahienne F de Oliveira, Giovani C Verissimo da Costa, Paulo M Bisch, Jose Hamilton Matheus Nascimento
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. Isolated rat hearts were submitted to IPC (three cycles of 5 min I/R) before 30-min global ischaemia and 60-min reperfusion...
September 2017: Basic Research in Cardiology
https://www.readbyqxmd.com/read/28688054/erratum-to-differential-regulation-of-protein-phosphatase-1-pp1-isoforms-in-human-heart-failure-and-atrial-fibrillation
#2
Stefanie Meyer-Roxlau, Simon Lämmle, Annett Opitz, Stephan Künzel, Julius P Joos, Stefan Neef, Karolina Sekeres, Samuel Sossalla, Friedrich Schöndube, Konstantin Alexiou, Lars S Maier, Dobromir Dobrev, Kaomei Guan, Silvio Weber, Ali El-Armouche
No abstract text is available yet for this article.
September 2017: Basic Research in Cardiology
https://www.readbyqxmd.com/read/28688053/animal-models-of-arrhythmogenic-right-ventricular-cardiomyopathy-what-have-we-learned-and-where-do-we-go-insight-for-therapeutics
#3
REVIEW
Laura Padrón-Barthe, Fernando Domínguez, Pablo Garcia-Pavia, Enrique Lara-Pezzi
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...
September 2017: Basic Research in Cardiology
https://www.readbyqxmd.com/read/28656319/erratum-to-impairment-of-ph-gradient-and-membrane-potential-mediates-redox-dysfunction-in-the-mitochondria-of-the-post-ischemic-heart
#4
Patrick T Kang, Chwen-Lih Chen, Paul Lin, William M Chilian, Yeong-Renn Chen
No abstract text is available yet for this article.
July 2017: Basic Research in Cardiology
https://www.readbyqxmd.com/read/28647906/exogenous-gdf11-induces-cardiac-and-skeletal-muscle-dysfunction-and-wasting
#5
Teresa A Zimmers, Yanling Jiang, Meijing Wang, Tiffany W Liang, Joseph E Rupert, Ernie D Au, Francesco E Marino, Marion E Couch, Leonidas G Koniaris
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. Mice were injected with GDF11 secreting cells, an identical model to that used to initially identify the in vivo effects of myostatin...
July 2017: Basic Research in Cardiology
https://www.readbyqxmd.com/read/28639003/the-crucial-role-of-activin-a-alk4-pathway-in-the-pathogenesis-of-ang-ii-induced-atrial-fibrosis-and-vulnerability-to-atrial-fibrillation
#6
Qian Wang, Ying Yu, Pengpai Zhang, Yihe Chen, Changyi Li, Jie Chen, Yuepeng Wang, Yigang Li
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...
July 2017: Basic Research in Cardiology
https://www.readbyqxmd.com/read/28624975/deleterious-acute-and-chronic-effects-of-bradycardic-right-ventricular-apex-pacing-consequences-for-arrhythmic-outcome
#7
T R G Stams, A Dunnink, W M van Everdingen, H D M Beekman, R van der Nagel, B Kok, M F A Bierhuizen, M J Cramer, M Meine, M A Vos
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...
July 2017: Basic Research in Cardiology
https://www.readbyqxmd.com/read/28612156/reduction-of-sr-ca-2-leak-and-arrhythmogenic-cellular-correlates-by-smp-114-a-novel-camkii-inhibitor-with-oral-bioavailability
#8
Stefan Neef, Christian Mann, Anne Zwenger, Nataliya Dybkova, Lars S Maier
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...
July 2017: Basic Research in Cardiology
https://www.readbyqxmd.com/read/28612155/the-role-of-spatial-organization-of-ca-2-release-sites-in-the-generation-of-arrhythmogenic-diastolic-ca-2-release-in-myocytes-from-failing-hearts
#9
Andriy E Belevych, Hsiang-Ting Ho, Ingrid M Bonilla, Radmila Terentyeva, Karsten E Schober, Dmitry Terentyev, Cynthia A Carnes, Sándor Györke
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...
July 2017: Basic Research in Cardiology
https://www.readbyqxmd.com/read/28597249/differential-regulation-of-protein-phosphatase-1-pp1-isoforms-in-human-heart-failure-and-atrial-fibrillation
#10
Stefanie Meyer-Roxlau, Simon Lämmle, Annett Opitz, Stephan Künzel, Julius P Joos, Stefan Neef, Karolina Sekeres, Samuel Sossalla, Friedrich Schöndube, Konstantin Alexiou, Lars S Maier, Dobromir Dobrev, Kaomei Guan, Silvio Weber, Ali El-Armouche
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. Recent evidence from animal models implicated previously unrecognized, isoform-specific activities of PP1 in the healthy and diseased heart. Therefore, this study examined the expression of the distinct PP1 isoforms PP1α, β, and γ in human heart failure (HF) and atrial fibrillation (AF) and addressed the consequences of β-adrenoceptor blocker (beta-blocker) therapy for HF patients with reduced ejection fraction on PP1 isoform expression...
July 2017: Basic Research in Cardiology
https://www.readbyqxmd.com/read/28540528/sema3a-promotes-the-resolution-of-cardiac-inflammation-after-myocardial-infarction
#11
Marieke Rienks, Paolo Carai, Nicole Bitsch, Mark Schellings, Maarten Vanhaverbeke, Johan Verjans, Ilona Cuijpers, Stephane Heymans, Anna Papageorgiou
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. In mice, the expression of Sema3A also increases in response to myocardial ischemia being expressed by infiltrating leukocytes...
July 2017: Basic Research in Cardiology
https://www.readbyqxmd.com/read/28540527/alignment-of-inducible-vascular-progenitor-cells-on-a-micro-bundle-scaffold-improves-cardiac-repair-following-myocardial-infarction
#12
Anurag Jamaiyar, Weiguo Wan, Vahagn Ohanyan, Molly Enrick, Danielle Janota, Devan Cumpston, Hokyung Song, Kelly Stevanov, Christopher L Kolz, Tatev Hakobyan, Feng Dong, Bi-Min Zhang Newby, William M Chilian, Liya Yin
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. We tested a new approach of stem cell therapy by delivery of induced vascular progenitor cells (iVPCs) grown on polymer micro-bundle scaffolds in a rat model of myocardial infarction...
July 2017: Basic Research in Cardiology
https://www.readbyqxmd.com/read/28534119/splenic-ly6c-hi-monocytes-contribute-to-adverse-late-post-ischemic-left-ventricular-remodeling-in-heme-oxygenase-1-deficient-mice
#13
Mateusz Tomczyk, Izabela Kraszewska, Krzysztof Szade, Karolina Bukowska-Strakova, Marco Meloni, Alicja Jozkowicz, Jozef Dulak, Agnieszka Jazwa
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). Nevertheless, its importance in timely resolution of post-ischemic inflammation remains incompletely understood. The aim of this study was to determine the role of Hmox1 in the monocyte/macrophage-mediated cardiac remodeling in a mouse model of MI...
July 2017: Basic Research in Cardiology
https://www.readbyqxmd.com/read/28534118/exercise-induced-circulating-extracellular-vesicles-protect-against-cardiac-ischemia-reperfusion-injury
#14
Yihua Bei, Tianzhao Xu, Dongchao Lv, Pujiao Yu, Jiahong Xu, Lin Che, Avash Das, John Tigges, Vassilios Toxavidis, Ionita Ghiran, Ravi Shah, Yongqin Li, Yuhui Zhang, Saumya Das, Junjie Xiao
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. We subsequently identified that serum EVs were increased by ~1.85-fold in mice after 3-week swimming. Intramyocardial injection of equivalent quantities of EVs from exercised mice and non-exercised controls provided similar protective effects against acute ischemia/reperfusion (I/R) injury in mice...
July 2017: Basic Research in Cardiology
https://www.readbyqxmd.com/read/28526910/expression-and-regulation-of-type-2a-protein-phosphatases-and-alpha4-signalling-in-cardiac-health-and-hypertrophy
#15
Olga Eleftheriadou, Andrii Boguslavskyi, Michael R Longman, Jonathan Cowan, Asvi Francois, Richard J Heads, Brian E Wadzinski, Ali Ryan, Michael J Shattock, Andrew K Snabaitis
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)...
July 2017: Basic Research in Cardiology
https://www.readbyqxmd.com/read/28508960/impairment-of-ph-gradient-and-membrane-potential-mediates-redox-dysfunction-in-the-mitochondria-of-the-post-ischemic-heart
#16
Patrick T Kang, Chwen-Lih Chen, Paul Lin, William M Chilian, Yeong-Renn Chen
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. Here we studied mitochondria from the risk region of rat hearts subjected to 30 min of coronary ligation and 24 h of reperfusion in vivo...
July 2017: Basic Research in Cardiology
https://www.readbyqxmd.com/read/28492973/fast-therapeutic-hypothermia-prevents-post-cardiac-arrest-syndrome-through-cyclophilin-d-mediated-mitochondrial-permeability-transition-inhibition
#17
Vincent Jahandiez, Martin Cour, Thomas Bochaton, Maryline Abrial, Joseph Loufouat, Abdallah Gharib, Annie Varennes, Michel Ovize, Laurent Argaud
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. Adult male New Zealand White rabbits underwent 15 min of CA followed by 120 min of reperfusion...
July 2017: Basic Research in Cardiology
https://www.readbyqxmd.com/read/28478479/dissecting-the-role-of-myeloid-and-mesenchymal-fibroblasts-in-age-dependent-cardiac-fibrosis
#18
JoAnn Trial, Celia Pena Heredia, George E Taffet, Mark L Entman, Katarzyna A Cieslik
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. Some of the monocytes that migrate into the heart polarize into M2a macrophages/myeloid fibroblasts. The number of activated mesenchymal fibroblasts also increases with age, and consequently, both sources of fibroblasts contribute to fibrosis...
July 2017: Basic Research in Cardiology
https://www.readbyqxmd.com/read/28439731/il-10-improves-cardiac-remodeling-after-myocardial-infarction-by-stimulating-m2-macrophage-polarization-and-fibroblast-activation
#19
Mira Jung, Yonggang Ma, Rugmani Padmanabhan Iyer, Kristine Y DeLeon-Pennell, Andriy Yabluchanskiy, Michael R Garrett, Merry L Lindsey
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...
May 2017: Basic Research in Cardiology
https://www.readbyqxmd.com/read/28439730/physiological-and-therapeutic-regulation-of-pcsk9-activity-in-cardiovascular-disease
#20
REVIEW
Simon Glerup, Rainer Schulz, Ulrich Laufs, Klaus-Dieter Schlüter
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...
May 2017: Basic Research in Cardiology
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