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https://www.readbyqxmd.com/read/28434633/echocardiographic-evaluation-of-left-ventricular-mass-index-in-children-with-hypospadias-after-hormonal-stimulation-with-topical-testosterone-a-randomized-controlled-trial
#1
Elisabeth Campos de Andrade, Kelly Christina de Castro Paiva, Sarah da Silva Guedes, Mariana Lima C Souza, Marina Novellino Pereira, Laura Pimenta Miana, André Avarese de Figueiredo, José de Bessa, José Murillo B Netto
INTRODUCTION: Testosterone is often used in the preoperative period of hypospadias surgery. Previous studies have demonstrated the presence of androgen receptors in cardiac myocytes that can modulate the phenotype. The use of supraphysiological doses of androgens can lead to toxicity on the heart muscle and, in some cases, to left ventricular hypertrophy. This randomized double blind controlled clinical trial aims to evaluate the effect of topical testosterone on left ventricular mass index in boys with hypospadias...
April 10, 2017: Journal of Pediatric Urology
https://www.readbyqxmd.com/read/28432434/ventricular-androgenic-anabolic-steroid-related-remodeling-an-immunohistochemical-study
#2
Rossana Cecchi, Barbara Muciaccia, Costantino Ciallella, Natale Mario Di Luca, Akihiko Kimura, Cristina Sestili, Mizuho Nosaka, Toshikazu Kondo
BACKGROUND: Several fatal cases of bodybuilders, following a myocardial infarction after long exposure to androgenic-anabolic steroids (AAS), are reported. In recent years, evidence has emerged of cases of heart failure related to AAS consumption, with no signs of coronary or aorta atherosclerosis. This study aims to further investigate the pathogenesis of the ventricular AAS-related remodeling performing immunohistochemistry (IHC). METHOD: In order to examine innate immunity activity and myocytes and endothelial cell apoptosis, IHC analyses were performed on heart tissue of two cases of bodybuilders who died after years of supratherapeutic use of metelonone and nandrolone and where no atherosclerosis or thrombosis were found, using the following antibodies: anti-CD68, anti-iNOS, anti-CD163, anti-CD 15, anti-CD8, anti-CD4, anti-HIF1 α, and in situ TUNEL staining...
April 21, 2017: International Journal of Legal Medicine
https://www.readbyqxmd.com/read/28432058/mk5-haplodefficiency-attenuates-hypertrophy-and-preserves-diastolic-function-during-remodeling-induced-by-chronic-pressure-overload-in-the-mouse-heart
#3
Sherin Nawaito, Dharmendra Dingar, Pramod Sahadevan, Bahira Hussein, Fatiha Sahmi, Yanfen Shi, Marc-Antoine Gillis, Matthias Gaestel, Jean-Claude Tardif, Bruce G Allen
MK5 is a protein serine and threonine kinase that is activated by p38 MAPK and the atypical MAPKs ERK3 and ERK4. The physiological function(s) of MK5 remain unknown. Herein we examine the effect of MK5 haplodeficiency on cardiac function and myocardial remodeling. At 12-weeks of age, MK5 haplodeficient mice (MK5(+/-)) were smaller than age-matched wild-type litter mates (MK5(+/+)), with similar diastolic function but reduced systolic function. Transverse aortic constriction (TAC) was employed to induce a chronic pressure overload in twelve-week-old male MK5(+/-) and MK5(+/+) mice...
April 21, 2017: American Journal of Physiology. Heart and Circulatory Physiology
https://www.readbyqxmd.com/read/28430892/anti-arrhythmic-potential-of-the-late-sodium-current-inhibitor-gs-458967-in-murine-scn5a-1798insd-and-human-scn5a-1795insd-ipsc-derived-cardiomyocytes
#4
Vincent Portero, Simona Casini, Maaike Hoekstra, Arie O Verkerk, Isabella Mengarelli, Luiz Belardinelli, Sridharan Rajamani, Arthur A M Wilde, Connie R Bezzina, Marieke W Veldkamp, Carol Ann Remme
AIM: Selective inhibition of cardiac late sodium current (INaL) is an emerging target in the treatment of ventricular arrhythmias. We investigated the electrophysiological effects of GS-458967 (GS967), a potent, selective inhibitor of INaL, in an overlap syndrome model of both gain and loss of sodium channel function, comprising cardiomyocytes derived from both human SCN5A-1795insD+/- induced pluripotent stem cells (hiPSC-CMs) and mice carrying the homologous mutation Scn5a-1798insD+/-...
April 18, 2017: Cardiovascular Research
https://www.readbyqxmd.com/read/28430882/inhibition-of-the-cardiac-myocyte-mineralocorticoid-receptor-ameliorates-doxorubicin-induced-cardiotoxicity
#5
Achim Lother, Stella Bergemann, Jessica Kowalski, Michael Huck, Ralf Gilsbach, Christoph Bode, Lutz Hein
Aim: HASH(0x459a6f0) Anthracyclines such as doxorubicin are widely used in cancer therapy but their use is limited by cardiotoxicity. Up to date there is no established strategy for the prevention of anthracyclin-induced heart failure. In this study, we evaluated the role of the cardiac myocyte mineralocorticoid receptor (MR) during doxorubicin-induced cardiotoxicity. Methods and results: HASH(0x459b1d0) A single high-dose or repetitive low-dose doxorubicin administration lead to markedly reduced left ventricular function in mice...
April 18, 2017: Cardiovascular Research
https://www.readbyqxmd.com/read/28428622/inhibition-of-late-sodium-current-suppresses-calcium-related-ventricular-arrhythmias-by-reducing-the-phosphorylation-of-camk-ii-and-sodium-channel-expressions
#6
Xiao-Hong Wei, Shan-Dong Yu, Lu Ren, Si-Hui Huang, Qiao-Mei Yang, Ping Wang, Yan-Peng Chu, Wei Yang, Yan-Sheng Ding, Yong Huo, Lin Wu
Cardiac arrhythmias associated with intracellular calcium inhomeostasis are refractory to antiarrhythmic therapy. We hypothesized that late sodium current (I Na) contributed to the calcium-related arrhythmias. Monophasic action potential duration at 90% completion of repolarization (MAPD90) was significantly increased and ventricular arrhythmias were observed in hearts with increased intracellular calcium concentration ([Ca(2+)]i) by using Bay K 8644, and the increase became greater in hearts treated with a combination of ATX-II and Bay K 8644 compared to Bay K 8644 alone...
April 20, 2017: Scientific Reports
https://www.readbyqxmd.com/read/28428073/isosteviol-prevents-the-prolongation-of-action-potential-in-hypertrophied-cardiomyoctyes-by-regulating-transient-outward-potassium-and-l-type-calcium-channels
#7
Zhuo Fan, Nanying Lv, Xiao Luo, Wen Tan
Cardiac hypertrophy is a thickening of the heart muscle that is associated with cardiovascular diseases such as hypertension and myocardial infarction. It occurs initially as an adaptive process against increased workloads and often leads to sudden arrhythmic deaths. Studies suggest that the lethal arrhythmia is attributed to hypertrophy-induced destabilization of cardiac electrical activity, especially the prolongation of the action potential. The reduced activity of Ito is demonstrated to be responsible for the ionic mechanism of prolonged action potential duration and arrhythmogeneity...
April 17, 2017: Biochimica et Biophysica Acta
https://www.readbyqxmd.com/read/28425440/the-valosin-containing-protein-is-a-novel-mediator-of-mitochondrial-respiration-and-cell-survival-in-the-heart-in-vivo
#8
Paulo Lizano, Eman Rashed, Shaunrick Stoll, Ning Zhou, Hairuo Wen, Tristan T Hays, Gangjian Qin, Lai-Hua Xie, Christophe Depre, Hongyu Qiu
The valosin-containing protein (VCP) participates in signaling pathways essential for cell homeostasis in multiple tissues, however, its function in the heart in vivo remains unknown. Here we offer the first description of the expression, function and mechanism of action of VCP in the mammalian heart in vivo in both normal and stress conditions. By using a transgenic (TG) mouse with cardiac-specific overexpression (3.5-fold) of VCP, we demonstrate that VCP is a new and powerful mediator of cardiac protection against cell death in vivo, as evidenced by a 50% reduction of infarct size after ischemia/reperfusion versus wild type...
April 20, 2017: Scientific Reports
https://www.readbyqxmd.com/read/28422768/mechanisms-involved-in-secondary-cardiac-dysfunction-in-animal-models-of-trauma-and-haemorrhagic-shock
#9
Nick M Wilson, Johanna Wall, Veena Naganathar, Karim Brohi, Henry D De'Ath
Clinical evidence reveals the existence of a trauma induced secondary cardiac injury (TISCI) which is associated with poor patient outcomes. The mechanisms leading to TISCI in injured patients are uncertain. Conversely, animal models of trauma haemorrhage have repeatedly demonstrated significant cardiac dysfunction following injury, and highlighted mechanisms through which this might occur. The aim of this review was to provide an overview of the animal studies describing TISCI and its pathophysiology.Basic science models of trauma show evidence of innate immune system activation via Toll-Iike receptors (TLRs), the exact protagonists of which remain unclear...
April 18, 2017: Shock
https://www.readbyqxmd.com/read/28413954/computational-models-for-understanding-of-structure-function-and-pharmacology-of-the-cardiac-potassium-channel-kv11-1-herg
#10
Sören Wacker, Sergei Yu Noskov, Laura L Perissinotti
The rapid delayed rectifier current IKr is one of the major K+ currents involved into repolarization of the human cardiac action potential. Various inherited or drug-induced forms of the long QT syndrome (LQTS) in humans are linked to functional and structural modifications in the IKr conducting channels. IKr is carried by the potassium channel Kv11.1 encoded by the gene KCNH2 (commonly referred to as human ether-a-go-go-related gene or hERG) [1][2]. The first necessary step for predicting emergent drug effects on the heart is determining and modeling the binding thermodynamics and kinetics of primary and major off-target drug interactions with subcellular targets...
April 14, 2017: Current Topics in Medicinal Chemistry
https://www.readbyqxmd.com/read/28412414/endothelin-1-promotes-hypertrophic-remodelling-of-cardiac-myocytes-by-activating-sustained-signalling-and-transcription-downstream-of-endothelin-type-a-receptors
#11
Caroline R Archer, Emma L Robinson, Faye M Drawnel, H Llewelyn Roderick
G-protein coupled receptor (GPCR) mediated activation of the MAPK signalling cascade is a key pathway in the induction of hypertrophic remodelling of the heart - a response to pathological cues including hypertension and myocardial infarction. While levels of pro-hypertrophic hormone agonists of GPCRs increase during periods of greater workload to enhance cardiac output, hypertrophy does not necessarily result. Here we investigated the relationship between the duration of exposure to the pro-hypertrophic GPCR agonist endothelin-1 (ET-1) and the induction of hypertrophic remodelling in neonatal rat ventricular myocytes (NRVM) and in the adult rat heart in vivo...
April 13, 2017: Cellular Signalling
https://www.readbyqxmd.com/read/28410144/cardiotoxicity-in-oncology-and-coronary-microcirculation-future-challenges-in-theranostics
#12
Giovanni Peretto, Davide Lazzeroni, Carmem L Sartorio, Paolo G Camici
Many of the patients undergoing chemotherapy or radiotherapy for cancer are at increased risk of developing cardiovascular diseases. Recent evidence suggests that cardiac dysfunction and subsequent heart failure are mainly due to vascular toxicity rather than only to due to myocyte toxicity. However, not all of the vascular toxicity of cancer therapies can be explained by epicardial coronary artery disease. In fact, in the last decades, it has been found that myocardial ischemia may occur as a consequence of structural or functional dysfunction of the complex network of vessels, which cannot be seen by a coronary angiography: the coronary microcirculation...
June 1, 2017: Frontiers in Bioscience (Landmark Edition)
https://www.readbyqxmd.com/read/28408648/azithromycin-causes-a-novel-proarrhythmic-syndrome
#13
Zhenjiang Yang, Joseph K Prinsen, Kevin R Bersell, Wangzhen Shen, Liudmila Yermalitskaya, Tatiana Sidorova, Paula B Luis, Lynn Hall, Wei Zhang, Liping Du, Ginger Milne, Patrick Tucker, Alfred L George, Courtney M Campbell, Robert A Pickett, Christian M Shaffer, Nagesh Chopra, Tao Yang, Bjorn C Knollmann, Dan M Roden, Katherine T Murray
BACKGROUND: The widely used macrolide antibiotic azithromycin increases risk of cardiovascular and sudden cardiac death, although the underlying mechanisms are unclear. Case reports, including the one we document here, demonstrate that azithromycin can cause rapid, polymorphic ventricular tachycardia in the absence of QT prolongation, indicating a novel proarrhythmic syndrome. We investigated the electrophysiological effects of azithromycin in vivo and in vitro using mice, cardiomyocytes, and human ion channels heterologously expressed in human embryonic kidney (HEK 293) and Chinese hamster ovary (CHO) cells...
April 2017: Circulation. Arrhythmia and Electrophysiology
https://www.readbyqxmd.com/read/28408457/correction-to-%C3%AE-adrenergic-signaling-inhibits-gq-dependent-protein-kinase-d-activation-by-preventing-protein-kinase-d-translocation-and-multimodal-shg-2pf-imaging-of-microdomain-ca-2-contraction-coupling-in-live-cardiac-myocytes
#14
https://www.readbyqxmd.com/read/28407237/cytoskeletal-remodeling-and-regulation-of-cell-fate-in-the-hypertensive-neonatal-pulmonary-artery-in-response-to-stress
#15
REVIEW
Dina Johar
Neonatal pulmonary hypertension (PHN) is a lethal progressive disease that occurs in prenatal circulatory transition. Mechanical wall strain caused by cardiac pulsation integrates with hypoxia to generate rapidly progressive myocyte cytoskeleton disassembly and failure to exert force generation. The physiological responses to such an interaction have not been investigated. The persistent phenotype does not respond to traditional vasodilator therapy; hence, there is a need for new treatment strategies to improve the morbidity and mortality outcomes...
April 13, 2017: Journal of Cellular Physiology
https://www.readbyqxmd.com/read/28404615/myeloperoxidase-mediates-postischemic-arrhythmogenic-ventricular-remodeling
#16
Martin Mollenhauer, Kai Friedrichs, Max Lange, Jan Gesenberg, Lisa Remane, Christina Kerkenpaß, Jenny Krause, Johanna Schneider, Thorben Ravekes, Martina Maass, Marcel Halbach, Gabriel Peinkofer, Tomo Saric, Dennis Mehrkens, Matti Adam, Florian G Deuschl, Denise Lau, Birgit Geertz, Kashish Manchanda, Thomas Eschenhagen, Lukas Kubala, Tanja K Rudolph, Yuping Wu, Wh W Tang, Stanley L Hazen, Stephan Baldus, Anna Klinke, Volker Rudolph
Rationale: Ventricular arrhythmias remain the leading cause of death in patients suffering myocardial ischemia. Myeloperoxidase (MPO), a heme-enzyme released by polymorphonuclear neutrophils, accumulates within ischemic myocardium and has been linked to adverse left ventricular remodeling. Objective: To reveal the role of MPO for the development of ventricular arrhythmias. Methods and Results: In different murine models of myocardial ischemia MPO deficiency profoundly decreased vulnerability for ventricular tachycardia (VT) upon programmed right ventricular and burst stimulation and spontaneously as assessed by ECG telemetry following isoproterenol injection...
April 12, 2017: Circulation Research
https://www.readbyqxmd.com/read/28402883/a-role-of-bk-channel-in-regulation-of-ca-2-channel-in-ventricular-myocytes-by-substrate-stiffness
#17
Hucheng Zhao, Yang Yu, Xiaoan Wu, Sisi Liu, Bailin Liu, Jing Du, Bo Li, Linhua Jiang, Xiqiao Feng
Substrate stiffness is crucial for diverse cell functions, but the mechanisms conferring cells with mechanosensitivity are still elusive. By tailoring substrate stiffness with 10-fold difference, we showed that L-type voltage-gated Ca(2+) channel current density was greater in chick ventricular myocytes cultured on the stiff substrate than on the soft substrate. Blockage of the BK channel increased the Ca(2+) current density on the soft substrate and consequently eliminated substrate stiffness regulation of the Ca(2+) channel...
April 11, 2017: Biophysical Journal
https://www.readbyqxmd.com/read/28400398/multi-imaging-method-to-assay-the-contractile-mechanical-output-of-micropatterned-human-ipsc-derived-cardiac-myocytes
#18
Alexandre J Ribeiro, Olivier Schwab, Mohammad A Mandegar, Yen-Sin Ang, Bruce R Conklin, Deepak Srivastava, Beth L Pruitt
Rationale: During each beat, cardiac myocytes generate the mechanical output necessary for heart function through contractile mechanisms that involve shortening of sarcomeres along myofibrils. Human induced pluripotent stem cells can be differentiated into cardiac myocytes that model cardiac contractile mechanical output more robustly when micropatterned into physiological shapes. Quantifying the mechanical output of these cells enables us to assay cardiac activity in a dish. Objective: We sought to develop a computational platform that integrates analytical approaches to quantify the mechanical output of single micropatterned cardiac myocytes from microscopy videos...
April 11, 2017: Circulation Research
https://www.readbyqxmd.com/read/28396172/role-of-suppression-of-the-inward-rectifier-current-ik1-on-terminal-action-potential-repolarization-in-the-failing-heart
#19
Michael G Klein, Matie Shou, Jayna Stohlman, Soroosh Sohljoo, Myles Haigney, Richard R Tidwell, Robert E Goldstein, Thomas P Flagg, Mark C Haigney
BACKGROUND: The failing heart exhibits an increased arrhythmia susceptibility that is often attributed to action potential (AP) prolongation due to significant ion channel remodeling. IK1 has been reported to be reduced, but its contribution to shaping the AP waveform and cell excitability in the failing heart remains unclear. OBJECTIVE: To define the effect of IK1 suppression on the cardiac AP and excitability in the normal and failing heart. METHODS: We used electrophysiological and pharmacological approaches to investigate IK1 function in a swine tachy-pacing model of heart failure...
April 7, 2017: Heart Rhythm: the Official Journal of the Heart Rhythm Society
https://www.readbyqxmd.com/read/28394420/tiron-ameliorates-high-glucose-induced-cardiac-myocyte-apoptosis-by-pkc%C3%AE-dependent-inhibition-of-osteopontin
#20
Ping Jiang, Deling Zhang, Hong Qiu, Xianqi Yi, Yemin Zhang, Yingkang Cao, Bo Zhao, Zhongyuan Xia, Changhua Wang
Tiron functions as an effective antioxidant alleviating the intracellular reactive oxygen species (ROS) or the acute toxic metal overload. The previous studies have shown that cardiac myocyte apoptosis can be effectively inhibited by tiron administration in streptozotocin (STZ)-induced diabetic rats, primary neonatal rat cardiomyocytes (NRVMs), and H9c2 embryonic rat cardiomyocytes. However, the underlying signaling mechanism is ill-defined. In the present study, we found that tiron supplementation significantly inhibited apoptosis of high glucose (HG)-treated NRVMs and the left ventricular cardiomyocytes from STZ-diabetic rat, accompanied with a reduction of osteopontin (OPN) levels as well as an inhibition of PKCδ phosphorylation...
April 10, 2017: Clinical and Experimental Pharmacology & Physiology
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