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Basic Research in Cardiology

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https://www.readbyqxmd.com/read/29043508/the-role-of-pi3k%C3%AE-isoform-in-cardioprotection
#1
Xavier Rossello, Jaime A Riquelme, Zhenhe He, Stasa Taferner, Bart Vanhaesebroeck, Sean M Davidson, Derek M Yellon
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...
October 17, 2017: Basic Research in Cardiology
https://www.readbyqxmd.com/read/28965130/regulation-of-myocardial-oxygen-delivery-in-response-to-graded-reductions-in-hematocrit-role-of-k-channels
#2
Alexander M Kiel, Adam G Goodwill, Jillian N Noblet, April L Barnard, Daniel J Sassoon, Johnathan D Tune
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). Progressive hemodilution with Hespan resulted in an increase in coronary flow from 0.39 ± 0.05 to 1.63 ± 0.16 ml/min/g (P < 0...
September 30, 2017: Basic Research in Cardiology
https://www.readbyqxmd.com/read/28952016/the-impact-of-irreproducibility-and-competing-protection-from-p2y12-antagonists-on-the-discovery-of-cardioprotective-interventions
#3
REVIEW
Michael V Cohen, James M Downey
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. It appears that earlier clinical trials were often based on results from a single experimental laboratory, thus minimizing the importance of establishing reproducibility in multiple laboratories by multiple scientists and in multiple models...
September 26, 2017: Basic Research in Cardiology
https://www.readbyqxmd.com/read/28913715/oxidized-low-density-lipoprotein-oxldl-affects-load-free-cell-shortening-of-cardiomyocytes-in-a-proprotein-convertase-subtilisin-kexin-9-pcsk9-dependent-way
#4
Klaus-Dieter Schlüter, Annemarie Wolf, Martin Weber, Rolf Schreckenberg, Rainer Schulz
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. Adult rat ventricular cardiomyocytes were isolated and incubated for 24 h with oxLDL...
September 14, 2017: Basic Research in Cardiology
https://www.readbyqxmd.com/read/28913553/dual-inhibition-of-cathepsin-g-and-chymase-reduces-myocyte-death-and-improves-cardiac-remodeling-after-myocardial-ischemia-reperfusion-injury
#5
Bahman Hooshdaran, Mikhail A Kolpakov, Xinji Guo, Sonni A Miller, Tao Wang, Douglas G Tilley, Khadija Rafiq, Abdelkarim Sabri
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. This study investigated whether a dual inhibition of Cat.G and chymase influences cardiomyocyte injury and wound healing after experimental IR in mice...
September 14, 2017: Basic Research in Cardiology
https://www.readbyqxmd.com/read/28905113/influence-of-increased-heart-rate-and-aortic-pressure-on-resting-indices-of-functional-coronary-stenosis-severity
#6
Lorena Casadonte, Bart-Jan Verhoeff, Jan J Piek, Ed VanBavel, Jos A E Spaan, Maria Siebes
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. In 15 patients (55 ± 3% diameter stenosis) Pa, intracoronary pressure (Pd) and flow velocity were obtained at control, and during atrial pacing at 120 bpm, increased Pa (+30 mmHg) with intravenous phenylephrine (PE), and elevated Pa while pacing at sinus heart rate (PE + sHR)...
September 13, 2017: Basic Research in Cardiology
https://www.readbyqxmd.com/read/28887652/disruption-of-adenylyl-cyclase-type-5-mimics-exercise-training
#7
John J Guers, Jie Zhang, Sara C Campbell, Marko Oydanich, Dorothy E Vatner, Stephen F Vatner
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. Exercise performance, measured by maximal distance and work to exhaustion, was increased in exercise-trained WT to levels already attained in untrained AC5 KO...
September 8, 2017: Basic Research in Cardiology
https://www.readbyqxmd.com/read/28887629/microrna-143-promotes-cardiac-ischemia-mediated-mitochondrial-impairment-by-the-inhibition-of-protein-kinase-cepsilon
#8
Hong Hong, Ting Tao, Si Chen, Chaoqi Liang, Yue Qiu, Yuhong Zhou, Rong Zhang
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...
September 8, 2017: Basic Research in Cardiology
https://www.readbyqxmd.com/read/28871329/transforming-growth-factor-%C3%AE-mediated-cd44-stat3-signaling-contributes-to-the-development-of-atrial-fibrosis-and-fibrillation
#9
Shang-Hung Chang, Yung-Hsin Yeh, Jia-Lin Lee, Yu-Juei Hsu, Chi-Tai Kuo, Wei-Jan Chen
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. Treatment of cultured rat atrial fibroblasts with transforming growth factor-β (TGF-β, a key mediator of atrial fibrosis) led to a higher expression of hyaluronan (HA), CD44, STAT3, and collagen (a principal marker of fibrosis) than that of ventricular fibroblasts...
September 4, 2017: Basic Research in Cardiology
https://www.readbyqxmd.com/read/28864889/methylglyoxal-derived-advanced-glycation-end-products-contribute-to-negative-cardiac-remodeling-and-dysfunction-post-myocardial-infarction
#10
Nick J R Blackburn, Branka Vulesevic, Brian McNeill, Cagla Eren Cimenci, Ali Ahmadi, Mayte Gonzalez-Gomez, Aleksandra Ostojic, Zhiyuan Zhong, Michael Brownlee, Paul J Beisswenger, Ross W Milne, Erik J Suuronen
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). MI was induced in GLO1 mice and wild-type (WT) littermates. At 6 h post-MI, mass spectrometry revealed that MG-H1 (a principal MG-AGE) was increased in the hearts of WT mice, and immunohistochemistry demonstrated that this persisted for 4 weeks...
September 1, 2017: Basic Research in Cardiology
https://www.readbyqxmd.com/read/28756533/long-term-spironolactone-treatment-reduces-coronary-trpc-expression-vasoconstriction-and-atherosclerosis-in-metabolic-syndrome-pigs
#11
Wennan Li, Xingjuan Chen, Ashley M Riley, S Christopher Hiett, Constance J Temm, Eleni Beli, Xin Long, Saikat Chakraborty, Mouhamad Alloosh, Fletcher A White, Maria B Grant, Michael Sturek, Alexander G Obukhov
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. MetS coronary arteries exhibited significant atherosclerosis, endothelial dysfunction, and increased histamine-induced contractions...
September 2017: Basic Research in Cardiology
https://www.readbyqxmd.com/read/28721633/erratum-to-exogenous-gdf11-induces-cardiac-and-skeletal-muscle-dysfunction-and-wasting
#12
Teresa A Zimmers, Yanlin Jiang, Meijing Wang, Tiffany W Liang, Joseph E Rupert, Ernie D Au, Francesco E Marino, Marion E Couch, Leonidas G Koniaris
No abstract text is available yet for this article.
September 2017: Basic Research in Cardiology
https://www.readbyqxmd.com/read/28695353/cardioprotection-by-the-transfer-of-coronary-effluent-from-ischaemic-preconditioned-rat-hearts-identification-of-cardioprotective-humoral-factors
#13
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
#14
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
#15
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/28861604/cardiac-optogenetics-using-light-to-monitor-cardiac-physiology
#16
REVIEW
Charlotte D Koopman, Wolfram H Zimmermann, Thomas Knöpfel, Teun P de Boer
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...
August 31, 2017: Basic Research in Cardiology
https://www.readbyqxmd.com/read/28819685/cardiomyocyte-dimethylarginine-dimethylaminohydrolase-1-ddah1-plays-an-important-role-in-attenuating-ventricular-hypertrophy-and-dysfunction
#17
Xin Xu, Ping Zhang, Dongmin Kwak, John Fassett, Wenhui Yue, Dorothee Atzler, Xinli Hu, Xiaohong Liu, Huan Wang, Zhongbing Lu, Haipeng Guo, Edzard Schwedhelm, Rainer H Böger, Peijie Chen, Yingjie Chen
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. While NO signaling is important for cardiac adaptation to stress, DDAH1 impact on cardiomyocyte homeostasis is not clear. Here we used the MerCreMer-LoxP model to specifically disrupt cardiomyocyte DDAH1 expression in adult mice to determine the physiological impact of cardiomyocyte DDAH1 under basal conditions and during hypertrophic stress imposed by transverse aortic constriction (TAC)...
August 17, 2017: Basic Research in Cardiology
https://www.readbyqxmd.com/read/28730386/erratum-to-changes-of-myocardial-gene-expression-and-protein-composition-in-patients-with-dilated-cardiomyopathy-after-immunoadsorption-with-subsequent-immunoglobulin-substitution
#18
Sabine Ameling, Gourav Bhardwaj, Elke Hammer, Daniel Beug, Leif Steil, Yvonne Reinke, Kerstin Weitmann, Markus Grube, Christiane Trimpert, Karin Klingel, Reinhard Kandolf, Wolfgang Hoffmann, Matthias Nauck, Marcus Dörr, Klaus Empen, Stephan B Felix, Uwe Völker
No abstract text is available yet for this article.
July 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
#19
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
#20
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
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