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https://www.readbyqxmd.com/read/28649439/mechanisms-of-action-of-sacubitril-valsartan-on-cardiac-remodeling-a-systems-biology-approach
#1
Oriol Iborra-Egea, Carolina Gálvez-Montón, Santiago Roura, Isaac Perea-Gil, Cristina Prat-Vidal, Carolina Soler-Botija, Antoni Bayes-Genis
Sacubitril/Valsartan, proved superiority over other conventional heart failure management treatments, but its mechanisms of action remains obscure. In this study, we sought to explore the mechanistic details for Sacubitril/Valsartan in heart failure and post-myocardial infarction remodeling, using an in silico, systems biology approach. Myocardial transcriptome obtained in response to myocardial infarction in swine was analyzed to address post-infarction ventricular remodeling. Swine transcriptome hits were mapped to their human equivalents using Reciprocal Best (blast) Hits, Gene Name Correspondence, and InParanoid database...
2017: NPJ Systems Biology and Applications
https://www.readbyqxmd.com/read/28649367/nitric-oxide-signalling-and-neuronal-nitric-oxide-synthase-in-the-heart-under-stress
#2
REVIEW
Yin Hua Zhang
Nitric oxide (NO) is an imperative regulator of the cardiovascular system and is a critical mechanism in preventing the pathogenesis and progression of the diseased heart. The scenario of bioavailable NO in the myocardium is complex: 1) NO is derived from both endogenous NO synthases (endothelial, neuronal, and/or inducible NOSs [eNOS, nNOS, and/or iNOS]) and exogenous sources (entero-salivary NO pathway) and the amount of NO from exogenous sources varies significantly; 2) NOSs are located at discrete compartments of cardiac myocytes and are regulated by distinctive mechanisms under stress; 3) NO regulates diverse target proteins through different modes of post-transcriptional modification (soluble guanylate cyclase [sGC]/cyclic guanosine monophosphate [cGMP]/protein kinase G [PKG]-dependent phosphorylation, S-nitrosylation, and transnitrosylation); 4) the downstream effectors of NO are multidimensional and vary from ion channels in the plasma membrane to signalling proteins and enzymes in the mitochondria, cytosol, nucleus, and myofilament; 5) NOS produces several radicals in addition to NO (e...
2017: F1000Research
https://www.readbyqxmd.com/read/28648628/impact-of-titin-strain-on-the-cardiac-slow-force-response
#3
REVIEW
Younss Ait-Mou, Mengjie Zhang, Jody L Martin, Marion L Greaser, Pieter P de Tombe
Stretch of myocardium, such as occurs upon increased filling of the cardiac chamber, induces two distinct responses: an immediate increase in twitch force followed by a slower increase in twitch force that develops over the course of several minutes. The immediate response is due, in part, to modulation of myofilament Ca(2+) sensitivity by sarcomere length (SL). The slowly developing force response, termed the Slow Force Response (SFR), is caused by a slowly developing increase in intracellular Ca(2+) upon sustained stretch...
June 22, 2017: Progress in Biophysics and Molecular Biology
https://www.readbyqxmd.com/read/28648627/myofilament-protein-dynamics-modulate-ead-formation-in-human-hypertrophic-cardiomyopathy
#4
REVIEW
Melanie A Zile, Natalia A Trayanova
Patients with hypertrophic cardiomyopathy (HCM), a disease associated with sarcomeric protein mutations, often suffer from sudden cardiac death (SCD) resulting from arrhythmia. In order to advance SCD prevention strategies, our understanding of how sarcomeric mutations in HCM patients contribute to enhanced arrhythmogenesis needs to be improved. Early afterdepolarizations (EADs) are an important mechanism underlying arrhythmias associated with HCM-SCD. Although the ionic mechanisms underlying EADs have been studied in general, whether myofilament protein dynamics mechanisms also underlie EADs remains unknown...
June 22, 2017: Progress in Biophysics and Molecular Biology
https://www.readbyqxmd.com/read/28648626/mechanosensitivity-of-microdomain-calcium-signalling-in-the-heart
#5
REVIEW
Patrick Schönleitner, Uli Schotten, Gudrun Antoons
In cardiac myocytes, calcium (Ca(2+)) signalling is tightly controlled in dedicated microdomains. At the dyad, i.e. the narrow cleft between t-tubules and junctional sarcoplasmic reticulum (SR), many signalling pathways combine to control Ca(2+)-induced Ca(2+) release during contraction. Local Ca(2+) gradients also exist in regions where SR and mitochondria are in close contact to regulate energetic demands. Loss of microdomain structures, or dysregulation of local Ca(2+) fluxes in cardiac disease, is often associated with oxidative stress, contractile dysfunction and arrhythmias...
June 22, 2017: Progress in Biophysics and Molecular Biology
https://www.readbyqxmd.com/read/28646979/inhibition-of-rapid-delayed-rectifier-potassium-current-ikr-by-ischemia-reperfusion-and-its-recovery-by-vitamin-e-in-ventricular-myocytes
#6
Yaoxu Chen, Chunxia Yin, Yingying Yang, Zhuo Fan, Jinling Shang, Wen Tan
Ischemia/reperfusion (I/R) induces prolongation of QT interval and action potential duration (APD), which is a major cardiac electrical disorder in patients with arrhythmias. However, the mechanism of QT interval prolongation induced by I/R remains unclear. In the present study, we hypothesized that the rapid component of delayed rectifier potassium (IKr) channel plays an important role in I/R-induced QT interval prolongation. We observed a marked attenuation of IKr and a significant prolongation of action potential duration (APD) in a simulated I/R system with sodium dithionite (Na2S2O4) in ventricular myocytes of guinea pigs...
July 2017: Journal of Electrocardiology
https://www.readbyqxmd.com/read/28646025/remodeling-of-repolarization-and-arrhythmia-susceptibility-in-a-myosin-binding-protein-c-knockout-mouse-model
#7
Amir Toib, Chen Zhang, Giulia Borghetti, Xiaoxiao Zhang, Markus Wallner, Yijun Yang, Constantine Troupes, Hajime Kubo, Thomas Sharp, Eric Feldsott, Remus M Berretta, Neil Zalavadia, Danielle Trappanese, Shavonn Harper, Polina Gross, Xiongwen Chen, Sadia Mohsin, Steven Houser
Hypertrophic cardiomyopathy (HCM) is one of the most common genetic cardiac diseases and amongst the leading causes of sudden cardiac death (SCD) in the young. The cellular mechanisms leading to SCD in HCM are not well known. Prolongation of the action potential duration (APD) is a common feature predisposing hypertrophied hearts to SCD. Previous studies have explored the roles of inward Na(+) and Ca(2+) in the development of HCM, but the role of repolarizing K(+) currents have not been defined. The objective of this study was to characterize the arrhythmogenic phenotype and cellular electrophysiological properties of mice with HCM, induced by Myosin Binding Protein C (MyBPC) Knockout (KO) and to test the hypothesis that remodeling of repolarizing K(+) currents cause APD prolongation in MyBPC KO myocytes...
June 23, 2017: American Journal of Physiology. Heart and Circulatory Physiology
https://www.readbyqxmd.com/read/28644868/electrophysiological-alterations-in-a-murine-model-of-chronic-coxsackievirus-b3-myocarditis
#8
Sven Kaese, Robert Larbig, Matthias Rohrbeck, Gerrit Frommeyer, Dirk Dechering, Jan Olligs, Sabine Schönhofer-Merl, Rainer Wessely, Karin Klingel, Guiscard Seebohm, Lars Eckardt
INTRODUCTION: Coxsackievirus B3 (CVB3) is known to induce acute and chronic myocarditis. Most infections are clinically unapparent but some patients suffer from ventricular arrhythmias (VA) and sudden cardiac death (SCD). Studies showed that acute CVB3 infection may cause impaired function of cardiac ion channels, creating a proarrhythmic substrate. However, it is unknown whether low level CVB3+ expression in myocytes may cause altered cardiac electrophysiology leading to VA. METHODS: Cellular electrophysiology was used to analyze cellular action potentials (APs) and occurrence of afterdepolarizations from isolated cardiomyocytes of wildtype (WT) and transgenic CVB3ΔVP0 (CVB3+) mice...
2017: PloS One
https://www.readbyqxmd.com/read/28643438/knockdown-of-mtfp1-can-minimize-doxorubicin-cardiotoxicity-by-inhibiting-dnm1l-mediated-mitochondrial-fission
#9
Lynn H H Aung, Ruibei Li, Bellur S Prabhakar, Peifeng Li
The long-term usage of doxorubicin (DOX) is largely limited due to the development of severe cardiomyopathy. Many studies indicate that DOX-induced cardiac injury is related to reactive oxygen species generation and ultimate activation of apoptosis. The role of novel mitochondrial fission protein 1 (Mtfp1) in DOX-induced cardiotoxicity remains elusive. Here, we report the pro-mitochondrial fission and pro-apoptotic roles of Mtfp1 in DOX-induced cardiotoxicity. DOX up-regulates the Mtfp1 expression in HL-1 cardiac myocytes...
June 23, 2017: Journal of Cellular and Molecular Medicine
https://www.readbyqxmd.com/read/28643198/urokinase-plasminogen-activator-protects-cardiac-myocytes-from-oxidative-damage-and-apoptosis-via-hogg1-induction
#10
Philipp J Hohensinner, Nikol Takacs, Christoph Kaun, Barbara Thaler, Konstantin A Krychtiuk, Stefan Pfaffenberger, Arezu Aliabadi, Andreas Zuckermann, Kurt Huber, Johann Wojta
The role of uPA in tissue remodeling and cell migration is already well established. In addition, uPA was reported to stabilize p53, a key cell cycle control, DNA repair and apoptosis initiation protein. We aimed to determine the role of uPA-uPAR signaling towards cell survival or apoptosis in human adult cardiac myocytes (HACM). HACM were stimulated with uPA and DNA damage was inflicted by incubating cells with 200 µM H2O2. To analyze for apoptotic cells we applied TUNEL staining. Oxidative damage foci were analyzed by staining for 8-oxoguanine base pairs...
June 22, 2017: Apoptosis: An International Journal on Programmed Cell Death
https://www.readbyqxmd.com/read/28642708/myricitrin-protects-cardiomyocytes-from-hypoxia-reoxygenation-injury-involvement-of-heat-shock-protein-90
#11
Min Wang, Gui-Bo Sun, Yu-Yang Du, Yu Tian, Ping Liao, Xue-Song Liu, Jing-Xue Ye, Xiao-Bo Sun
Modulation of oxidative stress is therapeutically effective in ischemia/reperfusion (I/R) injury. Myricitrin, a naturally occurring phenolic compound, is a potent antioxidant. However, little is known about its effect on I/R injury to cardiac myocytes. The present study was performed to investigate the potential protective effect of myricitrin against hypoxia/reoxygenation (H/R)-induced H9c2 cardiomyocyte injury and its underlying mechanisms. Myricitrin pretreatment improved cardiomyocyte viability, inhibited ROS generation, maintained the mitochondrial membrane potential, reduced apoptotic cardiomyocytes, decreased the caspase-3 activity, upregulated antiapoptotic proteins and downregulated proapoptotic proteins during H/R injury...
2017: Frontiers in Pharmacology
https://www.readbyqxmd.com/read/28642276/dedifferentiation-proliferation-and-redifferentiation-of-adult-mammalian-cardiomyocytes-after-ischemic-injury
#12
Wei Eric Wang, Liangpeng Li, Xuewei Xia, Wenbin Fu, Qiao Liao, Cong Lan, Dezhong Yang, Hongmei Chen, Rongchuan Yue, Cindy S Zeng, Lin Zhou, Bin Zhou, Dayue D Duan, Xiongwen Chen, Steven R Houser, Chunyu Zeng
Background -Adult mammalian hearts have a limited ability to generate new cardiomyocytes. Proliferation of existing adult cardiomyocytes (ACM) is a potential source of new cardiomyocytes. Understanding the fundamental biology of ACM proliferation could be of great clinical significance for treating myocardial infarction (MI). We aim to understand the process and regulation of ACM proliferation and its role in new cardiomyocyte formation of post-MI mouse hearts. Methods -β-actin-GFP transgenic mice and fate-mapping Myh6-MerCreMer-tdTomato/lacZ mice were used to trace the fate of ACMs...
June 22, 2017: Circulation
https://www.readbyqxmd.com/read/28641008/hypoxia-induced-changes-in-the-fibroblast-secretome-exosome-and-whole-cell-proteome-using-cultured-cardiac-derived-cells-isolated-from-neonatal-mice
#13
Jake Cosme, Hongbo Guo, Sina Hadipour-Lakmehsari, Andrew Emili, Anthony O Gramolini
Cardiac fibroblasts (CF) represent a major subpopulation of cells in the developing and adult heart. Cardiomyocyte (CM) and CF intercellular communication occurs through paracrine interactions and modulate myocyte development and stress response. Detailed proteomic analysis of the CF secretome in normal and stressed conditions may offer insights into the role of CF in heart development and disease. Primary neonatal mouse CF were isolated and cultured for 24h in 21% (normoxic) or 2% (hypoxic) O2. Conditioned media was separated to obtain EXO and EXO-depleted secretome fractions...
June 22, 2017: Journal of Proteome Research
https://www.readbyqxmd.com/read/28640452/role-of-epicardial-adipose-tissue-in-health-and-disease-a-matter-of-fat
#14
Bénédicte Gaborit, Coralie Sengenes, Patricia Ancel, Alexis Jacquier, Anne Dutour
Epicardial adipose tissue (EAT) is a small but very biologically active ectopic fat depot that surrounds the heart. Given its rapid metabolism, thermogenic capacity, unique transcriptome, secretory profile, and simply measurability, epicardial fat has drawn increasing attention among researchers attempting to elucidate its putative role in health and cardiovascular diseases. The cellular crosstalk between epicardial adipocytes and cells of the vascular wall or myocytes is high and suggests a local role for this tissue...
June 18, 2017: Comprehensive Physiology
https://www.readbyqxmd.com/read/28637870/cardiac-myocyte-p38%C3%AE-kinase-regulates-angiogenesis-via-myocyte-endothelial-cell-cross-talk-during-stress-induced-remodeling-in-heart
#15
Beth A Rose, Tomohiro Yokota, Vishnu Chintalgattu, Shuxun Ren, Luisa Iruela-Arispe, Aarif Y Khakoo, Susumu Minamisawa, Yibin Wang
Stress-induced p38 mitogen-activated protein kinase (MAPK) activity is implicated in pathological remodeling in the heart. For example, constitutive p38 MAPK activation in cardiomyocytes induces pathological features, including myocyte hypertrophy, apoptosis, contractile dysfunction, and fetal gene expression. However, the physiological function of cardiomyocyte p38 MAPK activity in beneficial compensatory vascular remodeling is unclear. This report investigated the functional role and the underlying mechanisms of cardiomyocyte p38 MAPK activity in cardiac remodeling induced by chronic stress...
June 21, 2017: Journal of Biological Chemistry
https://www.readbyqxmd.com/read/28637784/tnfr2-stimulation-promotes-mitochondrial-fusion-via-stat3-and-nf-kb-dependent-activation-of-opa1-expression
#16
Jinliang Nan, Hengxun Hu, Yong Sun, Lianlian Zhu, Yingchao Wang, Zhiwei Zhong, Jing Zhao, Na Zhang, Ya Wang, Yaping Wang, Jian Ye, Ling Zhang, Xinyang Hu, Wei Zhu, Jian'an Wang
Rationale: Mitochondria are important cellular organelles and play essential roles in maintaining cell structure and function. Emerging evidence indicates that in addition to having pro-inflammatory and pro-apoptotic effects, tumor necrosis factor α (TNFα) can, under certain circumstances, promote improvements in mitochondrial integrity and function, phenomena that can be ascribed to the existence of TNFα receptor 2 (TNFR2). Objective: The present study aimed to investigate whether and how TNFR2 activation mediates the effects of TNFα on mitochondria...
June 21, 2017: Circulation Research
https://www.readbyqxmd.com/read/28637782/the-brugada-syndrome-susceptibility-gene-hey2-modulates-cardiac-transmural-ion-channel-patterning-and-electrical-heterogeneity
#17
Christiaan C Veerman, Svitlana Podliesna, Rafik Tadros, Elisabeth M Lodder, Isabella Mengarelli, Berend de Jonge, Leander Beekman, Julien Barc, Ronald Wilders, Arthur A Wilde, Bastiaan J Boukens, Ruben Coronel, Arie Verkerk, Carol Ann Remme, Connie R Bezzina
Rationale: Genome-wide association studies previously identified an association of rs9388451 at chromosome 6q22.3 (near HEY2) with Brugada syndrome (BrS). The causal gene and underlying mechanism remain unresolved. Objective: We used an integrative approach entailing transcriptomic studies in human hearts and electrophysiological studies in Hey2 heterozygous knockout mice (Hey2(+/-) ) to dissect the underpinnings of the 6q22.31 association with BrS. Methods and Results: We queried expression quantitative trait locus (eQTL) data acquired in 190 human left ventricular (LV) samples from the Genotype-Tissue Expression (GTEx) consortium for cis-eQTL effects of rs9388451 which revealed an association between BrS risk allele dosage and HEY2 expression (β=+0...
June 21, 2017: Circulation Research
https://www.readbyqxmd.com/read/28637196/chronological-change-of-right-ventricle-by-chronic-intermittent-hypoxia-in-mice
#18
Hyung-Ju Cho, Woon Heo, Jung Woo Han, Yong Hyuk Lee, Jin Myung Park, Min Jung Kang, Joo-Heon Yoon, Min Goo Lee, Chang-Hoon Kim, Joo Young Kim
Study Objective: No studies have investigated sequential changes in the heart on MRI, along with observation of functional lung phenotypes and genetics, over the duration of chronic intermittent hypoxia (CIH). We investigated chronological changes in heart and lung phenotypes after CIH using a mouse model to provide new insights into the pathophysiology of sleep apnea-induced cardiovascular disease. Methods: C57BL/6J adult male mice were randomized to 4 weeks or 8 weeks of CIH...
June 20, 2017: Sleep
https://www.readbyqxmd.com/read/28635626/adiponectin-a-therapeutic-target-for-obesity-diabetes-and-endothelial-dysfunction
#19
REVIEW
Arunkumar E Achari, Sushil K Jain
Adiponectin is the most abundant peptide secreted by adipocytes, whose reduction plays a central role in obesity-related diseases, including insulin resistance/type 2 diabetes and cardiovascular disease. In addition to adipocytes, other cell types, such as skeletal and cardiac myocytes and endothelial cells, can also produce this adipocytokine. Adiponectin effects are mediated by adiponectin receptors, which occur as two isoforms (AdipoR1 and AdipoR2). Adiponectin has direct actions in liver, skeletal muscle, and the vasculature...
June 21, 2017: International Journal of Molecular Sciences
https://www.readbyqxmd.com/read/28633090/pulmonary-and-cardiac-pathology-in-sudden-unexpected-death-in-epilepsy-sudep
#20
REVIEW
Fábio A Nascimento, Zian H Tseng, Cristian Palmiere, Joseph J Maleszewski, Takayuki Shiomi, Aileen McCrillis, Orrin Devinsky
OBJECTIVE: To review studies on structural pulmonary and cardiac changes in SUDEP cases as well as studies showing pulmonary or cardiac structural changes in living epilepsy patients. METHODS: We conducted electronic literature searches using the PubMed database for articles published in English, regardless of publication year, that included data on cardiac and/or pulmonary structural abnormalities in SUDEP cases or in living epilepsy patients during the postictal period...
June 17, 2017: Epilepsy & Behavior: E&B
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