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Condition: Arrhythmia

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Total 29 results found since Jan 2013.

Microglial Mincle receptor in the PVN contributes to sympathetic hyperactivity in acute myocardial infarction rat.
Abstract Malignant ventricular arrhythmias (VAs) following myocardial infarction (MI) is a lethal complication resulting from sympathetic nerve hyperactivity. Numerous evidence have shown that inflammation within the paraventricular nucleus (PVN) participates in sympathetic hyperactivity. Our aim was to explore the role of Macrophage-inducible C-type lectin (Mincle) within the PVN in augmenting sympathetic activity following MI,and whether NOD-like receptor family pyrin domain-containing 3 (NLRP3) inflammasome/IL-1β axis is involved in this activity. MI was induced by coronary artery ligation. Mincle expression l...
Source: J Cell Mol Med - October 24, 2018 Category: Molecular Biology Authors: Wang Y, Yin J, Wang C, Hu H, Li X, Xue M, Liu J, Cheng W, Wang Y, Li Y, Shi Y, Tan J, Li X, Liu F, Liu Q, Yan S Tags: J Cell Mol Med Source Type: research

Knockdown of Ift88 in fibroblasts causes extracellular matrix remodeling and decreases conduction velocity in cardiomyocyte monolayers
Conclusion: Disruption of cilia formation by siIft88 causes ECM remodeling and conduction abnormalities. Prevention of cilia loss could be a target for prevention of arrhythmias.
Source: Frontiers in Physiology - November 17, 2022 Category: Physiology Source Type: research

NOS1AP modulates intracellular Ca(2+) in cardiac myocytes and is up-regulated in dystrophic cardiomyopathy.
Authors: Treuer AV, Gonzalez DR Abstract NOS1AP gene (nitric oxide synthase 1-adaptor protein) is strongly associated with abnormalities in the QT interval of the electrocardiogram and with sudden cardiac death. To determine the role of NOS1AP in the physiology of the cardiac myocyte, we assessed the impact of silencing NOS1AP, using siRNA, on [Ca(2+)]i transients in neonatal cardiomyocytes. In addition, we examined the co-localization of NOS1AP with cardiac ion channels, and finally, evaluated the expression of NOS1AP in a mouse model of dystrophic cardiomyopathy. Using siRNA, NOS1AP levels were reduced to ~30% of...
Source: International Journal of Physiology, Pathophysiology and Pharmacology - November 16, 2014 Category: Physiology Tags: Int J Physiol Pathophysiol Pharmacol Source Type: research

Transcriptional regulation of stress kinase JNK2 in pro-arrhythmic CaMKII δ expression in the aged atrium
ConclusionJNK2 activation up-regulates CaMKII δ expression in the aged atrium. This JNK2 regulation in CaMKIIδ expression occurs at the transcription level through the JNK downstream transcription factor c-jun. The discovery of this novel molecular mechanism of JNK2-regulated CaMKII expression sheds new light on possible anti-arrhythmia drug development.
Source: Cardiovascular Research - January 19, 2018 Category: Cardiology Source Type: research

The activation of the G protein-coupled estrogen receptor (GPER) prevents and regresses cardiac hypertrophy
Publication date: Available online 28 December 2019Source: Life SciencesAuthor(s): Romina A. Di Mattia, Juan I.E. Mariángelo, Paula G. Blanco, Carolina Jaquenod De Giusti, Enrique L. Portiansky, Cecilia B. Mundiña-Weilenmann, Ernesto A. Aiello, Alejandro OrlowskiAbstractVentricular hypertrophy is a risk factors for arrhythmias, ischemia and sudden death. It involves cellular modifications leading to a pathological remodeling and is associated with heart failure. The activation of the G protein-coupled estrogen receptor (GPER) mediates beneficial actions in the cardiovascular system. Our goal was to prevent and regress th...
Source: Life Sciences - December 30, 2019 Category: Biology Source Type: research

Beneficial Effect of Edoxaban on Preventing Atrial Fibrillation and Coagulation by Reducing Inflammation via HBG1/HBD Biomarkers
Conclusion: Edoxaban could prevent atrial fibrillation and coagulation by reducing inflammation, lipids, and fibrosis via HBG1/HBD biomarkers effectively, and the effect was superior to that of rivaroxaban.
Source: Frontiers in Pharmacology - June 3, 2022 Category: Drugs & Pharmacology Source Type: research

Matrine induces caspase-independent program cell death in hepatocellular carcinoma through bid-mediated nuclear translocation of apoptosis inducing factor
The objective of this study was to investigate the major determinant for the cell death induced by matrine in human hepatocellular carcinoma. We use human hepatocellular carcinoma cell line HepG2 and human hepatocellular carcinoma xenograft in nude mice as models to study the action of matrine in hepatocellular cancers. We found that caspase-dependent and -independent Program Cell Death (PCD) occurred in matrine-treated HepG2 cells, accompanied by the decreasing of mitochondrial transmembrane potential and the increasing ROS production. Further studies showed that AIF released from the mitochondria to the nucleus, and sile...
Source: Molecular Cancer - March 16, 2014 Category: Cancer & Oncology Authors: Huan ZhouMinying XuYa GaoZhigang DengHanwei CaoWenqing ZhangQiao WangBing ZhangGang SongYanyan ZhanTianhui Hu Source Type: research

Ketoconazole induces apoptosis in rat cardiomyocytes through reactive oxygen species-mediated parkin overexpression.
Abstract Azole antifungals such as ketoconazole are generally known to induce a variety of heart function side effects, e.g., long-QT syndrome and ventricular arrhythmias. However, a clear mechanism for the action of ketoconazole in heart cells has not been reported. In the present study, we assessed the correlation between ketoconazole-induced apoptosis and the alteration of genes in response to ketoconazole in rat cardiomyocytes. Cardiomyocyte viability was significantly inhibited by treatment with ketoconazole. Ketoconazole also stimulated H2O2 generation and TUNEL-positive apoptosis in a dose-dependent manner....
Source: Archives of Toxicology - March 19, 2015 Category: Toxicology Authors: Won KJ, Lee KP, Yu S, Lee D, Lee DY, Lee HM, Kim J, Jung SH, Baek S, Kim B Tags: Arch Toxicol Source Type: research

Deletion of Kvβ1.1 subunit leads to electrical and hemodynamic changes causing cardiac hypertrophy in female murine hearts
This article is protected by copyright. All rights reserved
Source: Experimental Physiology - January 1, 2016 Category: Physiology Authors: Jared Tur, Kalyan C. Chapalamadugu, Timothy Padawer, Sachin L. Badole, Peter J. Kilfoil II, Aruni Bhatnagar, Srinivas M. Tipparaju Tags: Research Paper Source Type: research

PANCR, the PITX2 Adjacent Noncoding RNA, Is Expressed in Human Left Atria and Regulates PITX2c Expression Original Articles
Conclusions— PANCR and PITX2c are coordinately expressed early during cardiomyocyte differentiation from stem cells. PANCR knockdown decreased PITX2c expression in differentiated cardiomyocytes, altering the transcriptome in a manner similar to PITX2c knockdown.
Source: Circulation: Arrhythmia and Electrophysiology - January 18, 2016 Category: Cardiology Authors: Gore-Panter, S. R., Hsu, J., Barnard, J., Moravec, C. S., Van Wagoner, D. R., Chung, M. K., Smith, J. D. Tags: Arrhythmias, Atrial Fibrillation, Gene Expression & Regulation, Functional Genomics Original Articles Source Type: research

Bufalin derivative BF211 inhibits proteasome activity in human lung cancer cells in vitro by inhibiting β1 subunit expression and disrupting proteasome assembly.
CONCLUSION: BF211 inhibits proteasome activity in A549 cells by decreasing β1 subunit expression and disrupting proteasome assembly. PMID: 27238210 [PubMed - as supplied by publisher]
Source: Acta Pharmacologica Sinica - May 29, 2016 Category: Drugs & Pharmacology Authors: Sun P, Feng LX, Zhang DM, Liu M, Liu W, Mi T, Wu WY, Jiang BH, Yang M, Hu LH, Guo DA, Liu X Tags: Acta Pharmacol Sin Source Type: research

Aldosterone and Store-operated Ca2+ Channels Cell Biology
Store-operated Ca2+ entry (SOCE) has emerged as an important mechanism in cardiac pathology. However, the signals that up-regulate SOCE in the heart remain unexplored. Clinical trials have emphasized the beneficial role of mineralocorticoid receptor (MR) signaling blockade in heart failure and associated arrhythmias. Accumulated evidence suggests that the mineralocorticoid hormone aldosterone, through activation of its receptor, MR, might be a key regulator of Ca2+ influx in cardiomyocytes. We thus assessed whether and how SOCE involving transient receptor potential canonical (TRPC) and Orai1 channels are regulated by aldo...
Source: Journal of Biological Chemistry - June 16, 2016 Category: Chemistry Authors: Sabourin, J., Bartoli, F., Antigny, F., Gomez, A. M., Benitah, J.-P. Tags: Cell Biology Source Type: research

Contribution of two pore potassium channels to cardiac ventricular action potential revealed using human iPSC-derived cardiomyocytes.
Abstract Two pore potassium channels (K2p) have been described in modulating background conductance as leak channels in different physiological systems. In the heart, the expression of K2p channels is heterogeneous with equivocation regarding their functional role. Our objective was to determine the K2p expression profile and their physiological and pathophysiological contribution to cardiac electrophysiology. Induced pluripotent stem cells (iPSC) cells generated from humans were differentiated into cardiomyocytes (iPSC-CM). mRNA was isolated from these cells, commercial iPSC-CM (iCells®), control human heart ven...
Source: American Journal of Physiology. Heart and Circulatory Physiology - March 24, 2017 Category: Physiology Authors: Chai S, Wan X, Nassal DM, Liu H, Moravec CS, Ramirez-Navarro A, Deschenes I Tags: Am J Physiol Heart Circ Physiol Source Type: research

Readthrough of SCN5A Nonsense Mutations R1623X and S1812X Question Gene-therapy in Brugada Syndrome.
CONCLUSIONS: These results demonstrated that readthrough-enhancing methods effectively suppressed nonsense mutations in SCN5A and restored the expression of full-length channels. But the restored channels may increase the risk of arrhythmia. The strategies for nonsense mutations suppression provides potential evidence for personalized medicine for the treatment of genetic disorders. PMID: 28552050 [PubMed - as supplied by publisher]
Source: Current Gene Therapy - May 28, 2017 Category: Genetics & Stem Cells Authors: Teng S, Huang J, Gao Z, Hao J, Yang Y, Zhang S, Pu J, Hui R, Wu Y, Fan Z Tags: Curr Gene Ther Source Type: research

Current state of the art for cardiac arrhythmia gene therapy
Publication date: Available online 19 June 2017 Source:Pharmacology & Therapeutics Author(s): J. Kevin Donahue Cardiac arrhythmias are a leading cause of morbidity and mortality. Currently available therapeutic options lack sufficient efficacy and safety. Gene therapy has been proposed for treatment of cardiac arrhythmias. This review will discuss the current state of development for arrhythmia gene therapy. So far, all published studies are short-term, proof-of-concept animal studies. Potential replacement of cardiac pacemakers has been shown for combination gene therapy using the HCN2 gene and either the gene fo...
Source: Pharmacology and Therapeutics - June 20, 2017 Category: Drugs & Pharmacology Source Type: research