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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
#1
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/28551783/mitochondrial-mutations-in-cardiac-disorders
#2
Sung Ryul Lee, Jin Han
Mitochondria individually encapsulate their own genome, unlike other cellular organelles. Mitochondrial DNA (mtDNA) is a circular, double-stranded, 16,569-base paired DNA containing 37 genes: 13 proteins of the mitochondrial respiratory chain, two ribosomal RNAs (rRNAs; 12S and 16S), and 22 transfer RNAs (tRNAs). The mtDNA is more vulnerable to oxidative modifications compared to nuclear DNA because of its proximity to ROS-producing sites, limited presence of DNA damage repair systems, and continuous replication in the cell...
2017: Advances in Experimental Medicine and Biology
https://www.readbyqxmd.com/read/28450904/camkii-the-molecular-villain-that-aggravates-cardiovascular-disease
#3
Peiying Zhang
Pathological remodeling of the myocardium is an integral part of the events that lead to heart failure (HF), which involves altered gene expression, disturbed signaling pathways and altered Ca(2+) homeostasis and the players involved in this process. Of particular interest is the chronic activation of Ca(2+)/calmodulin-dependent protein kinase II (CaMKII) isoforms in heart, which further aggravate the injury to myocardium. Expression and activity of CaMKII have been found to be elevated in various conditions of stressed myocardium and in different heart diseases in both animal models as well as heart patients...
March 2017: Experimental and Therapeutic Medicine
https://www.readbyqxmd.com/read/28369703/the-gap-junction-modifier-zp1609-decreases-cardiomyocyte-hypercontracture-following-ischaemia-reperfusion-independent-from-mitochondrial-connexin-43
#4
Kerstin Boengler, Marko Bulic, Rolf Schreckenberg, Klaus-Dieter Schlüter, Rainer Schulz
BACKGROUND AND PURPOSE: Dysregulation of gap junction-mediated cell coupling contributes to development of arrhythmias and myocardial damage after ischaemia/reperfusion (I/R). Connexin 43 (Cx43) is present at ventricular gap junctions and also in the mitochondria of cardiomyocytes. The dipeptide (2S, 4R)-1-(2-aminoacetyl)-4-benzamidopyrrolidine-2-carboxylic acid (ZP1609) has antiarrhythmic properties and reduces infarct size when given at reperfusion. However, it is unclear, whether ZP1609 targets Cx43-containing mitochondria and affects cardiomyocyte hypercontracture following I/R...
July 2017: British Journal of Pharmacology
https://www.readbyqxmd.com/read/28349259/effect-of-paroxetine-on-left-ventricular-remodeling-in-an-in-vivo-rat-model-of-myocardial-infarction
#5
Thomas Ravn Lassen, Jan Møller Nielsen, Jacob Johnsen, Steffen Ringgaard, Hans Erik Bøtker, Steen Buus Kristiansen
Left ventricular (LV) remodeling following a myocardial infarction (MI) involves formation of reactive oxygen species (ROS). Paroxetine, a selective serotonin reuptake inhibitor, has an antioxidant effect in the vascular wall. We investigated whether paroxetine reduces myocardial ROS formation and LV remodeling following a MI. In a total of 32 Wistar rats, MI was induced by a 30-min ligation of the left anterior descending artery followed by 7- or 28-day reperfusion. During the 28 days of reperfusion, LV remodeling was evaluated by magnetic resonance imaging (MRI) and echocardiography (n = 20)...
May 2017: Basic Research in Cardiology
https://www.readbyqxmd.com/read/28231545/aqueous-extract-of-cortex-dictamni-protects-h9c2-cardiomyocytes-from-hypoxia-reoxygenation-induced-oxidative-stress-and-apoptosis-by-pi3k-akt-signaling-pathway
#6
Lin Li, Yunfeng Zhou, Yanlin Li, Lili Wang, Lan Sun, Lidong Zhou, Hiderori Arai, Yun Qi, Yang Xu
Ischemia-reperfusion injury is the major manifestation of ischemic heart disease, which facilitates cardiac arrhythmias, heart failure and death. Oxidative stress and apoptosis have been involved in the pathogenesis of myocardial ischemia-reperfusion injury. Modern pharmacological studies have indicated that the extracts and active compounds of Cortex Dictamni exhibit antioxidative and cardiovascular protective activities. This study was designed to investigate the protective effect of aqueous extract of Cortex Dictamni (CDAE) on regulating hypoxia/reoxygenation (H/R)-induced cardiomyocytes oxidative stress and apoptosis...
May 2017: Biomedicine & Pharmacotherapy, Biomédecine & Pharmacothérapie
https://www.readbyqxmd.com/read/28126503/-pathophysiology-of-obstructive-sleep-apnea-syndrome-and-its-cardiometabolic-consequences
#7
Marie Destors, Renaud Tamisier, Louis-Marie Galerneau, Patrick Lévy, Jean-Louis Pepin
Obstructive sleep apnoea syndrome (OSAS) is characterized by recurrent partial or complete pharyngeal collapses during sleep. The pathophysiology of OSAS is complex and multifactorial. Factors influencing upper airway patency include a reduction in upper airway dimensions that can result from both anatomical and functional alterations (obesity, fluid shift or maxillo-facial structural changes), and increased pharyngeal collapsibility owing to reduced neuromuscular compensation and lack of the pharyngeal protective reflex during sleep...
January 23, 2017: La Presse Médicale
https://www.readbyqxmd.com/read/28105734/calcium-calmodulin-dependent-protein-kinase-mediates-the-intracellular-signalling-pathways-of-cardiac-apoptosis-in-mice-with-impaired-glucose-tolerance
#8
Marilen Federico, Enrique L Portiansky, Leandro Sommese, Francisco J Alvarado, Paula G Blanco, Carolina N Zanuzzi, John Dedman, Marcia Kaetzel, Xander H T Wehrens, Alicia Mattiazzi, Julieta Palomeque
KEY POINTS: Spontaneous sarcoplasmic reticulum (SR) Ca(2+) release events increased in fructose-rich diet mouse (FRD) myocytes vs. control diet (CD) mice, in the absence of significant changes in SR Ca(2+) load. In HEK293 cells, hyperglycaemia significantly enhanced [(3) H]ryanodine binding and Ca(2+) /calmodulin-dependent protein kinase II (CaMKII) phosphorylation of RyR2-S2814 residue vs. normoglycaemia. These increases were prevented by CaMKII inhibition. FRD significantly augmented cardiac apoptosis in WT vs...
June 15, 2017: Journal of Physiology
https://www.readbyqxmd.com/read/28098356/mechano-chemo-transduction-in-cardiac-myocytes
#9
Ye Chen-Izu, Leighton T Izu
The heart has the ability to adjust to changing mechanical loads. The Frank-Starling law and the Anrep effect describe exquisite intrinsic mechanisms the heart has for autoregulating the force of contraction to maintain cardiac output under changes of preload and afterload. Although these mechanisms have been known for more than a century, their cellular and molecular underpinnings are still debated. How does the cardiac myocyte sense changes in preload or afterload? How does the myocyte adjust its response to compensate for such changes? In cardiac myocytes Ca(2+) is a crucial regulator of contractile force and in this review we compare and contrast recent studies from different labs that address these two important questions...
June 15, 2017: Journal of Physiology
https://www.readbyqxmd.com/read/28096168/sk-channel-enhancers-attenuate-ca2-dependent-arrhythmia-in-hypertrophic-hearts-by-regulating-mito-ros-dependent-oxidation-and-activity-of-ryr
#10
Tae Yun Kim, Radmila Terentyeva, Karim H F Roder, Weiyan Li, Man Liu, Ian Greener, Shanna Hamilton, Iuliia Polina, Kevin R Murphy, Richard T Clements, Samuel C Dudley, Gideon Koren, Bum-Rak Choi, Dmitry Terentyev
Aims: Plasmamembrane small conductance Ca2+-activated K+ (SK) channels were implicated in ventricular arrhythmias in infarcted and failing hearts. Recently, SK channels were detected in the inner mitochondria membrane (IMM) (mSK), and their activation protected from acute ischaemia-reperfusion injury by reducing intracellular levels of reactive oxygen species (ROS). We hypothesized that mSK play an important role in regulating mitochondrial function in chronic cardiac diseases. We investigated the role of mSK channels in Ca2+-dependent ventricular arrhythmia using rat model of cardiac hypertrophy induced by banding of the ascending aorta thoracic aortic banding (TAB)...
March 1, 2017: Cardiovascular Research
https://www.readbyqxmd.com/read/27991911/inhibition-of-infarction-induced-sympathetic-innervation-with-endothelin-receptor-antagonism-via-a-pi3k-gsk-3%C3%AE-dependent-pathway
#11
T-M Lee, Nen-Chung Chang, Shinn-Zong Lin
Although endothelin (ET)-1 has been shown to upregulate nerve growth factor (NGF) expression, the molecular mechanisms are largely unknown. Phosphatidylinositol 3-kinase (PI3K)/Akt/glycogen synthase kinase (GSK)-3β signal has been implicated in the regulation of NGF. We investigated whether selective ET receptor blockers attenuated cardiac sympathetic reinnervation through restoring PI3K/Akt/GSK-3β activity. After ligation of the left anterior descending artery, male Wistar rats were randomized to either vehicle, atrasentan (an ETA receptor antagonist) or A-192621 (an ETB receptor antagonist) for 4 weeks...
December 19, 2016: Laboratory Investigation; a Journal of Technical Methods and Pathology
https://www.readbyqxmd.com/read/27932075/non-enzymatic-oxidized-metabolite-of-dha-4-rs-4-f4t-neuroprostane-protects-the-heart-against-reperfusion-injury
#12
Jérôme Roy, Jérémy Fauconnier, Camille Oger, Charlotte Farah, Claire Angebault-Prouteau, Jérôme Thireau, Patrice Bideaux, Valérie Scheuermann, Valérie Bultel-Poncé, Marie Demion, Jean-Marie Galano, Thierry Durand, Jetty Chung-Yung Lee, Jean-Yves Le Guennec
Acute myocardial infarction leads to an increase in oxidative stress and lipid peroxidation. 4(RS)-4-F4t-Neuroprostane (4-F4t-NeuroP) is a mediator produced by non-enzymatic free radical peroxidation of the cardioprotective polyunsaturated fatty acid, docosahexaenoic acid (DHA). In this study, we investigated whether intra-cardiac delivery of 4-F4t-NeuroP (0.03mg/kg) prior to occlusion (ischemia) prevents and protects rat myocardium from reperfusion damages. Using a rat model of ischemic-reperfusion (I/R), we showed that intra-cardiac infusion of 4-F4t-NeuroP significantly decreased infarct size following reperfusion (-27%) and also reduced ventricular arrhythmia score considerably during reperfusion (-41%)...
January 2017: Free Radical Biology & Medicine
https://www.readbyqxmd.com/read/27925238/danshen-enhanced-cardioprotective-effect-of-cardioplegia-on-ischemia-reperfusion-injury-in-a-human-induced-pluripotent-stem-cell-derived-cardiomyocytes-model
#13
Wei Wei, Yiwei Liu, Qiang Zhang, Yangming Wang, Xiaoling Zhang, Hao Zhang
Myocardial ischemia-reperfusion (I/R) injury is unavoidable during cardioplegic arrest and open-heart surgery. Danshen is one of the most popular traditional herbal medicines in China, which has entered the Food and Drug Administration-approved phase III clinical trial. This study was aimed to develop a human-induced pluripotent stem cell-derived cardiomyocytes (hiPSC-CMs) model to mimic I/R injury and evaluate the cardioprotective effect of regular cardioplegic solution with Danshen. hiPSC-CMs were cultured with the crystalloid cardioplegic solution (Thomas group) and Thomas solution with 2 or 10 µg/mL Danshen (Thomas plus Danshen groups)...
May 2017: Artificial Organs
https://www.readbyqxmd.com/read/27788262/resveratrol-reverses-functional-chagas-heart-disease-in-mice
#14
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
#15
Zhaokang Yang, Hannah M Kirton, Moza Al-Owais, Jérôme Thireau, Sylvain Richard, Chris Peers, Derek S Steele
AIMS: In the heart, β1-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. The aim of the present study was to investigate the influence of Epac2-Rap1 signaling on the heart using both in vivo and in vitro approaches...
October 27, 2016: Antioxidants & Redox Signaling
https://www.readbyqxmd.com/read/27536244/reactive-oxygen-species-endoplasmic-reticulum-stress-and-mitochondrial-dysfunction-the-link-with-cardiac-arrhythmogenesis
#16
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
#17
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
#18
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
#19
REVIEW
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
#20
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
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