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ROS and arrhythmias

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https://www.readbyqxmd.com/read/27788262/resveratrol-reverses-functional-chagas-heart-disease-in-mice
#1
Glaucia Vilar-Pereira, Vitor C Carneiro, Hilton Mata-Santos, Amanda R R Vicentino, Isalira P Ramos, Naira L L Giarola, Daniel F Feijó, José R Meyer-Fernandes, Heitor A Paula-Neto, Emiliano Medei, Marcelo T Bozza, Joseli Lannes-Vieira, Claudia N Paiva
Chronic chagasic cardiomyopathy (CCC) develops years after acute infection by Trypanosoma cruzi and does not improve after trypanocidal therapy, despite reduction of parasite burden. During disease, the heart undergoes oxidative stress, a potential causative factor for arrhythmias and contractile dysfunction. Here we tested whether antioxidants/ cardioprotective drugs could improve cardiac function in established Chagas heart disease. We chose a model that resembles B1-B2 stage of human CCC, treated mice with resveratrol and performed electrocardiography and echocardiography studies...
October 2016: PLoS Pathogens
https://www.readbyqxmd.com/read/27649969/epac2-rap1-signaling-regulates-reactive-oxygen-species-production-and-susceptibility-to-cardiac-arrhythmias
#2
Zhaokang Yang, Hannah Kirton, Moza Al-Owais, Jerôme Thireau, Sylvain Richard, Derek Steele, Chris Peers
AIMS: In the heart, β<sub>1</sub>-adrenergic signaling involves cyclic adenosine monophosphate (cAMP) acting via both protein kinase-A (PKA) and 'exchange protein directly activated by cAMP' (Epac): a guanine nucleotide exchange factor for the small GTPase Rap1. Inhibition of Epac-Rap1 signaling has been proposed as a therapeutic strategy for both cancer and cardiovascular disease. However, previous work suggests that impaired Rap1 signaling may have detrimental effects on cardiac function...
September 21, 2016: Antioxidants & Redox Signaling
https://www.readbyqxmd.com/read/27536244/reactive-oxygen-species-endoplasmic-reticulum-stress-and-mitochondrial-dysfunction-the-link-with-cardiac-arrhythmogenesis
#3
REVIEW
Gary Tse, Bryan P Yan, Yin W F Chan, Xiao Yu Tian, Yu Huang
BACKGROUND: Cardiac arrhythmias represent a significant problem globally, leading to cerebrovascular accidents, myocardial infarction, and sudden cardiac death. There is increasing evidence to suggest that increased oxidative stress from reactive oxygen species (ROS), which is elevated in conditions such as diabetes and hypertension, can lead to arrhythmogenesis. METHOD: A literature review was undertaken to screen for articles that investigated the effects of ROS on cardiac ion channel function, remodeling and arrhythmogenesis...
2016: Frontiers in Physiology
https://www.readbyqxmd.com/read/27434747/humanin-exerts-cardioprotection-against-cardiac-ischemia-reperfusion-injury-through-attenuation-of-mitochondrial-dysfunction
#4
Savitree Thummasorn, Nattayaporn Apaijai, Sasiwan Kerdphoo, Krekwit Shinlapawittayatorn, Siriporn C Chattipakorn, Nipon Chattipakorn
AIM: Myocardial reperfusion via the re-canalization of occluded coronary arteries is gold standard for the treatment of acute myocardial infarction. However, reperfusion itself can cause myocardial damage due to increased reactive oxygen species (ROS) production, a process known as ischemia/reperfusion (I/R) injury. Cardiac mitochondria are the major organelle of ROS production in the heart. Cardiac mitochondrial dysfunction caused by an increased ROS production can increase cardiac arrhythmia incidence, myocardial infarct size, and cardiac dysfunction...
December 2016: Cardiovascular Therapeutics
https://www.readbyqxmd.com/read/27342245/pathways-of-cardiac-toxicity-comparison-between-chemotherapeutic-drugs-doxorubicin-and-mitoxantrone
#5
REVIEW
Roberto Marques Damiani, Dinara Jaqueline Moura, Cassiana Macagnan Viau, Rafael Andrade Caceres, João Antonio Pêgas Henriques, Jenifer Saffi
Anthracyclines, e.g., doxorubicin (DOX), and anthracenediones, e.g., mitoxantrone (MTX), are drugs used in the chemotherapy of several cancer types, including solid and non-solid malignancies such as breast cancer, leukemia, lymphomas, and sarcomas. Although they are effective in tumor therapy, treatment with these two drugs may lead to side effects such as arrhythmia and heart failure. At the same clinically equivalent dose, MTX causes slightly reduced cardiotoxicity compared with DOX. These drugs interact with iron to generate reactive oxygen species (ROS), target topoisomerase 2 (Top2), and impair mitochondria...
September 2016: Archives of Toxicology
https://www.readbyqxmd.com/read/27230643/molecular-and-cellular-mechanisms-of-cardiovascular-disorders-in-diabetes
#6
Manasi S Shah, Michael Brownlee
The clinical correlations linking diabetes mellitus with accelerated atherosclerosis, cardiomyopathy, and increased post-myocardial infarction fatality rates are increasingly understood in mechanistic terms. The multiple mechanisms discussed in this review seem to share a common element: prolonged increases in reactive oxygen species (ROS) production in diabetic cardiovascular cells. Intracellular hyperglycemia causes excessive ROS production. This activates nuclear poly(ADP-ribose) polymerase, which inhibits GAPDH, shunting early glycolytic intermediates into pathogenic signaling pathways...
May 27, 2016: Circulation Research
https://www.readbyqxmd.com/read/27222313/inhibition-of-rac1-reduces-store-overload-induced-calcium-release-and-protects-against-ventricular-arrhythmia
#7
Lili Zhang, Xiangru Lu, Le Gui, Yan Wu, Stephen M Sims, Guoping Wang, Qingping Feng
Rac1 is a small GTPase and plays key roles in multiple cellular processes including the production of reactive oxygen species (ROS). However, whether Rac1 activation during myocardial ischaemia and reperfusion (I/R) contributes to arrhythmogenesis is not fully understood. We aimed to study the effects of Rac1 inhibition on store overload-induced Ca(2+) release (SOICR) and ventricular arrhythmia during myocardial I/R. Adult Rac1(f/f) and cardiac-specific Rac1 knockdown (Rac1(ckd) ) mice were subjected to myocardial I/R and their electrocardiograms (ECGs) were monitored for ventricular arrhythmia...
August 2016: Journal of Cellular and Molecular Medicine
https://www.readbyqxmd.com/read/26990944/remote-vs-local-ischaemic-preconditioning-in-the-rat-heart-infarct-limitation-suppression-of-ischaemic-arrhythmia-and-the-role-of-reactive-oxygen-species
#8
Michael M Galagudza, Dmitry L Sonin, Timur D Vlasov, Dmitry I Kurapeev, Eugene V Shlyakhto
The unmet clinical need for myocardial salvage during ischaemia-reperfusion injury requires the development of new techniques for myocardial protection. In this study the protective effect of different local ischaemic preconditioning (LIPC) and remote ischaemic preconditioning (RIPC) protocols was compared in the rat model of myocardial ischaemia-reperfusion, using infarct size and ischaemic tachyarrhythmias as end-points. In addition, the hypothesis that there is involvement of reactive oxygen species (ROS) in the protective signalling by RIPC was tested, again in comparison with LIPC...
February 2016: International Journal of Experimental Pathology
https://www.readbyqxmd.com/read/26981310/cellular-and-molecular-mechanisms-of-arrhythmia-by-oxidative-stress
#9
REVIEW
Ali A Sovari
Current therapies for arrhythmia using ion channel blockade, catheter ablation, or an implantable cardioverter defibrillator have limitations, and it is important to search for new antiarrhythmic therapeutic targets. Both atrial fibrillation and heart failure, a condition with increased arrhythmic risk, are associated with excess amount of reactive oxygen species (ROS). There are several possible ways for ROS to induce arrhythmia. ROS can cause focal activity and reentry. ROS alter multiple cardiac ionic currents...
2016: Cardiology Research and Practice
https://www.readbyqxmd.com/read/26980303/sulfur-dioxide-contributes-to-the-cardiac-and-mitochondrial-dysfunction-in-rats
#10
Guohua Qin, Meiqiong Wu, Jiaoxia Wang, Zhifang Xu, Jin Xia, Nan Sang
Epidemiological studies have demonstrated an association between sulfur dioxide (SO2) and an increase of morbidity and mortality of cardiovascular diseases, such as ischemic heart disease, heart failure, and arrhythmia. Mitochondrion is the most sensitive organelle in myocardium of animals exposed to SO2 Here we study the molecular characterization of mitochondrial dysfunction in cardiac muscles of rat after SO2 exposure. We found that the cytochrome c oxidase (COX) activity, mitochondrial membrane potential (ΔΨm), ATP contents, mitochondrial DNA (mtDNA) contents, and mRNA expression of complexes IV and V subunits encoded by mtDNA were decreased after NaHSO3 treatment in vitro or SO2 inhalation in vivo The mitochondrial dysfunctions were accompanied by depressions of co-activator of peroxisome proliferator activated receptor gamma (PGC-1α), nuclear respiratory factor 1, and mitochondrial transcription factor A (TFAM) mRNA and protein...
June 2016: Toxicological Sciences: An Official Journal of the Society of Toxicology
https://www.readbyqxmd.com/read/26940997/atorvastatin-blocks-increased-l-type-ca2-current-and-cell-injury-elicited-by-angiotensin-ii-via-inhibiting-oxide-stress
#11
Yanzhuo Ma, Lingfeng Kong, Shuying Qi, Dongmei Wang
Thel-type Ca(2+)current (ICa,l) plays a crucial role in shaping action potential and is involved in cardiac arrhythmia. Statins have been demonstrated to contribute to anti-apoptotic and anti-arrhythmic effects in the heart. Here, we examined whether atorvastatin regulates theICa,land cell injury induced by angiotensin II (AngII) as well as the putative intracellular cascade responsible for the effects. Cultured neonatal rat ventricular myocytes were incubated with AngII for 24 h, and then cell injury and expression levels of Nox2/gp91(phox), p47(phox) ,and Cav1...
April 2016: Acta Biochimica et Biophysica Sinica
https://www.readbyqxmd.com/read/26891434/-the-role-of-reactive-oxygen-species-ros-in-arrhythmogenesis
#12
REVIEW
Karol Tytman, Krzysztof Kaczmarek, Stanisława Lipińska, Jerzy K Wranicz
Reactive oxygen species (ROS) are the molecular oxygen derivatives that have at least one unpaired electron. Thus, ROS easily react with a number of cell structures causing a change in their functions. ROS produced in small quantities positively affect many cellular mechanisms, but in excess are responsible for the formation of oxidative stress. Oxidative stress is considered a major cause of many diseases, including cardiovascular disease. Abolition of the adverse effects of ROS on organisms in order to maintain redox homeostasis is possible thanks to antioxidants...
January 2016: Polski Merkuriusz Lekarski: Organ Polskiego Towarzystwa Lekarskiego
https://www.readbyqxmd.com/read/26880856/circulating-glutamate-and-taurine-levels-are-associated-with-the-generation-of-reactive-oxygen-species-in-paroxysmal-atrial-fibrillation
#13
Shintaro Takano, Kousuke Fujibayashi, Nakaba Fujioka, Ei-ichi Ueno, Minoru Wakasa, Yasuyuki Kawai, Kouji Kajinami
Atrial fibrillation (AF) is the most common cardiac arrhythmia, but its proarrhythmic mechanism remains to be elucidated. Glutamate (Glu) and taurine (Tau) are present in the myocardium at substantially higher concentrations than in the plasma, suggesting their active role in myocardium. Here, we tested the hypothesis that the metabolism of Glu and Tau is altered in association with the generation of reactive oxygen species (ROS) in patients with AF. Fifty patients with paroxysmal AF and 50 control subjects without a history of AF were consecutively enrolled...
2016: Disease Markers
https://www.readbyqxmd.com/read/26879900/%C3%AE-opioid-receptor-dor-signaling-and-reactive-oxygen-species-ros-mediate-intermittent-hypoxia-induced-protection-of-canine-myocardium
#14
Juan A Estrada, Arthur G Williams, Jie Sun, Leticia Gonzalez, H Fred Downey, James L Caffrey, Robert T Mallet
Intermittent, normobaric hypoxia confers robust cardioprotection against ischemia-induced myocardial infarction and lethal ventricular arrhythmias. δ-Opioid receptor (DOR) signaling and reactive oxygen species (ROS) have been implicated in cardioprotective phenomena, but their roles in intermittent hypoxia are unknown. This study examined the contributions of DOR and ROS in mediating intermittent hypoxia-induced cardioprotection. Mongrel dogs completed a 20 day program consisting of 5-8 daily, 5-10 min cycles of moderate, normobaric hypoxia (FIO2 0...
March 2016: Basic Research in Cardiology
https://www.readbyqxmd.com/read/26770648/protective-effect-of-peroxisome-proliferator-activated-receptor-%C3%AE-activation-against-cardiac-ischemia-reperfusion-injury-is-related-to-upregulation-of-uncoupling-protein-3
#15
Jong Wook Song, Hyo Jung Kim, Hyelin Lee, Jae-woo Kim, Young-Lan Kwak
Activation of peroxisome proliferator-activated receptor α (PPARα) confers cardioprotection, while its mechanism remains elusive. We investigated the protective effect of PPARα activation against cardiac ischemia-reperfusion injury in terms of the expression of uncoupling protein (UCP). Myocardial infarct size and UCP expression were measured in rats treated with WY-14643 20 mg/kg, a PPARα ligand, or vehicle. WY-14643 increased UCP3 expression in vivo. Myocardial infarct size was decreased in the WY-14643 group (76 ± 8% versus 42 ± 12%, P<0...
2016: Oxidative Medicine and Cellular Longevity
https://www.readbyqxmd.com/read/26588563/modeling-local-x-ros-and-calcium-signaling-in-the-heart
#16
Sarita Limbu, Tuan M Hoang-Trong, Benjamin L Prosser, W Jonathan Lederer, M Saleet Jafri
Stretching single ventricular cardiac myocytes has been shown experimentally to activate transmembrane nicotinamide adenine dinucleotide phosphate oxidase type 2 to produce reactive oxygen species (ROS) and increase the Ca2+ spark rate in a process called X-ROS signaling. The increase in Ca2+ spark rate is thought to be due to an increase in ryanodine receptor type 2 (RyR2) open probability by direct oxidation of the RyR2 protein complex. In this article, a computational model is used to examine the regulation of ROS and calcium homeostasis by local, subcellular X-ROS signaling and its role in cardiac excitation-contraction coupling...
November 17, 2015: Biophysical Journal
https://www.readbyqxmd.com/read/26555638/crosstalk-between-ryr2-oxidation-and-phosphorylation-contributes-to-cardiac-dysfunction-in-mice-with-duchenne-muscular-dystrophy
#17
Qiongling Wang, Wei Wang, Guoliang Wang, George G Rodney, Xander H T Wehrens
BACKGROUND: Patients with Duchenne muscular dystrophy (DMD) are at risk of developing cardiomyopathy and cardiac arrhythmias. Studies in a mouse model of DMD revealed that enhanced sarcoplasmic reticulum (SR) Ca(2+) leak contributes to the pathogenesis of cardiac dysfunction. In view of recent data suggesting the involvement of altered phosphorylation and oxidation of the cardiac ryanodine receptor (RyR2)/Ca(2+) release channel, we hypothesized that inhibition of RyR2 phosphorylation in a mouse model of DMD can prevent SR Ca(2+) leak by reducing RyR2 oxidation...
December 2015: Journal of Molecular and Cellular Cardiology
https://www.readbyqxmd.com/read/26503985/pivotal-role-of-mir-448-in-the-development-of-ros-induced-cardiomyopathy
#18
Sergii Kyrychenko, Viktoriia Kyrychenko, Myriam A Badr, Yoshiyuki Ikeda, Junichi Sadoshima, Natalia Shirokova
AIMS: Nicotinamide adenine dinucleotide oxidases (NOXs) are important contributors to cellular oxidative stress in the cardiovascular system. The NOX2 isoform is upregulated in numerous disorders, including dystrophic cardiomyopathy, where it drives the progression of the disease. However, mechanisms underlying NOX2 overexpression are still unknown. We investigated the role of microRNAs (miRs) in the regulation of NOX2 expression. METHODS AND RESULTS: Duchenne muscular dystrophy (DMD) was used as a model of cardiomyopathy...
December 1, 2015: Cardiovascular Research
https://www.readbyqxmd.com/read/26488649/increased-energy-demand-during-adrenergic-receptor-stimulation-contributes-to-ca-2-wave-generation
#19
Elisa Bovo, Stefan R Mazurek, Pieter P de Tombe, Aleksey V Zima
While β-adrenergic receptor (β-AR) stimulation ensures adequate cardiac output during stress, it can also trigger life-threatening cardiac arrhythmias. We have previously shown that proarrhythmic Ca(2+) waves during β-AR stimulation temporally coincide with augmentation of reactive oxygen species (ROS) production. In this study, we tested the hypothesis that increased energy demand during β-AR stimulation plays an important role in mitochondrial ROS production and Ca(2+)-wave generation in rabbit ventricular myocytes...
October 20, 2015: Biophysical Journal
https://www.readbyqxmd.com/read/26446751/detyrosinated-microtubules-modulate-mechanotransduction-in-heart-and-skeletal-muscle
#20
Jaclyn P Kerr, Patrick Robison, Guoli Shi, Alexey I Bogush, Aaron M Kempema, Joseph K Hexum, Natalia Becerra, Daniel A Harki, Stuart S Martin, Roberto Raiteri, Benjamin L Prosser, Christopher W Ward
In striated muscle, X-ROS is the mechanotransduction pathway by which mechanical stress transduced by the microtubule network elicits reactive oxygen species. X-ROS tunes Ca(2+) signalling in healthy muscle, but in diseases such as Duchenne muscular dystrophy (DMD), microtubule alterations drive elevated X-ROS, disrupting Ca(2+) homeostasis and impairing function. Here we show that detyrosination, a post-translational modification of α-tubulin, influences X-ROS signalling, contraction speed and cytoskeletal mechanics...
October 8, 2015: Nature Communications
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