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Condition: Arrhythmia

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Total 29 results found since Jan 2013.

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

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

mTORC1 is a key regulator that mediates OGD- and TGF β1-induced myofibroblast transformation and chondroitin-4-sulfate expression in cardiac fibroblasts
Exp Ther Med. 2022 Jun;23(6):413. doi: 10.3892/etm.2022.11340. Epub 2022 Apr 27.ABSTRACTIschemia-reperfusion infarct-derived chondroitin sulfate proteoglycans (CSPGs) are important for sustaining denervation of the infarct. Sympathetic denervation within the heart after myocardial infarction (MI) predicts the probability of a higher risk for serious ventricular arrhythmias. Chondroitin-4-sulfate (C4S) is the predominant chondroitin sulfate component in the heart. However, the mechanisms that induce CSPG expression in fibroblasts following MI remain to be elucidated. The present study found that oxygen-glucose deprivation (...
Source: Experimental and Therapeutic Medicine - May 23, 2022 Category: General Medicine Authors: Chao Li Zheng Zhang Yu Peng Yanying Zhang Wanrong Kang Yingdong Li Yang Hai Source Type: research

The Unfolded Protein Response as a Compensatory Mechanism and Potential Therapeutic Target in PLN R14del Cardiomyopathy
Conclusions: Together, these findings suggest that the UPR exerts a protective effect in the setting of PLN R14del cardiomyopathy and that modulation of the UPR might be exploited therapeutically.PMID:33928785 | DOI:10.1161/CIRCULATIONAHA.120.049844
Source: Circulation - April 30, 2021 Category: Cardiology Authors: Dries A M Feyen Isaac Perea-Gil Renee G C Maas Magdalena Harakalova Alexandra A Gavidia Jennifer Arthur Ataam Ting-Hsuan Wu Aryan Vink Jiayi Pei Nirmal Vadgama Albert J Suurmeijer Wouter P Te Rijdt Michelle Vu Prashila L Amatya Maricela Prado Yuan Zhang L Source Type: research

Silencing of CCR4-NOT complex subunits affects heart structure and function RESEARCH ARTICLE
This article has an associated First Person interview with the first author of the paper.
Source: DMM Disease Models and Mechanisms - July 19, 2020 Category: Biomedical Science Authors: Elmen, L., Volpato, C. B., Kervadec, A., Pineda, S., Kalvakuri, S., Alayari, N. N., Foco, L., Pramstaller, P. P., Ocorr, K., Rossini, A., Cammarato, A., Colas, A. R., Hicks, A. A., Bodmer, R. Tags: Stem Cells, Drosophila as a Disease Model RESEARCH ARTICLE 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

β-Arrestin2 regulates the rapid component of delayed rectifier K+ currents and cardiac action potential of guinea pig cardiomyocytes after adrenergic stimulation.
This study investigated the role of β-arrestin2 in the regulation of cardiac hERG/IKr potassium channel and AP during chronic adrenergic stimulation. Single left ventricular myocytes were isolated from guinea pig heart, and were transfected with adenovirus encoding β-arrestin2, or β-arrestin2 siRNA or an empty adenovirus. Cell cultures containing 10 nM isoproterenol, 1 nM phenylephrine or vehicle alone (control medium) were electro-physiologically examined after 48 h of incubation. Action potential duration at 50 and 90 % of repolarization (APD50 and APD90) were measured using whole-cell patch-clamp recording. Sustained...
Source: Cellular and Molecular Biology - December 29, 2019 Category: Molecular Biology Tags: Cell Mol Biol (Noisy-le-grand) Source Type: research

Lamin A/C Cardiomyopathy: Implications for Treatment
AbstractPurpose of ReviewThe purpose of this review is to provide an update on lamin A/C (LMNA)-related cardiomyopathy and discuss the current recommendations and progress in the management of this disease.LMNA-related cardiomyopathy, an inherited autosomal dominant disease, is one of the most common causes of dilated cardiomyopathy and is characterized by steady progression toward heart failure and high risks of arrhythmias and sudden cardiac death.Recent FindingsWe discuss recent advances in the understanding of the molecular mechanisms of the disease including altered cell biomechanics, which may represent novel therape...
Source: Current Cardiology Reports - November 25, 2019 Category: Cardiology Source Type: research

Plant-Derived Alkaloids: The Promising Disease-Modifying Agents for Inflammatory Bowel Disease
Conclusion This paper summarizes the current findings regarding the anti-colitis activity of plant-derived alkaloids and shows how these alkaloids exhibit significant and beneficial effects in alleviating colonic inflammation. These natural alkaloids are not only promising agents for IBD treatment but are also components for developing new wonder drugs. However, the underlying molecular mechanisms or toxicological evaluation of most plant-derived alkaloids still require much scientific research, and their actual efficacies for IBD patients have not been verified well in field research. Thus, further clinical trials to elu...
Source: Frontiers in Pharmacology - April 11, 2019 Category: Drugs & Pharmacology Source Type: research

LIM kinase 1 acts as a profibrotic mediator in permanent atrial fibrillation patients with valvular heart disease.
Abstract Atrial fibrillation (AF) is the most frequently diagnosed cardiac arrhythmia worldwide. Patients with permanent atrial fibrillation are at an increased risk of developing valvular heart disease. Atrial fibrosis occurs in this pathophysiological setting. LIM kinase 1 (LIMK1) is a serine/threonine kinase that regulates microtubule stability and actin polymerization in fibroblasts. LIMK1 has been implicated in the pathogenesis of atrial fibrillation. Clinical data and biopsies of the right atrial appendage were collected from 50 patients with valvular heart disease who underwent heart valve replacement surge...
Source: Journal of Biosciences - February 28, 2019 Category: Biomedical Science Authors: Chen Q, Gimple RC, Li G, Chen J, Wu H, Li R, Xie J, Xu B Tags: J Biosci Source Type: research

Novel role of the clustered miR-23b-3p and miR-27b-3p in enhanced expression of fibrosis-associated genes by targeting TGFBR3 in atrial fibroblasts.
This study aimed to investigate the role of the clustered miR-23b-3p and miR-27b-3p in atrial fibrosis. Human atrial fibroblasts (HAFs) were isolated from atrial appendage tissue of patients with sinus rhythm. A cell model of atrial fibrosis was achieved in Ang-II-induced HAFs. Cell proliferation and migration were detected. We found that miR-23b-3p and miR-27b-3p were markedly increased in atrial appendage tissues of AF patients and in Ang-II-treated HAFs. Overexpression of miR-23b-3p and miR-27b-3p enhanced the expression of collagen, type I, alpha 1 (COL1A1), COL3A1 and ACTA2 in HAFs without significant effects on their...
Source: J Cell Mol Med - February 7, 2019 Category: Molecular Biology Authors: Yang Z, Xiao Z, Guo H, Fang X, Liang J, Zhu J, Yang J, Li H, Pan R, Yuan S, Dong W, Zheng XL, Wu S, Shan Z Tags: J Cell Mol Med Source Type: research

Inhibition of microRNA-155 attenuates sympathetic neural remodeling following myocardial infarction via reducing M1 macrophage polarization and inflammatory responses in mice.
In conclusion, miR-155 inhibition downregulated NGF expression via decreasing M1 macrophage polarization and inflammatory responses dependent on the SOCS1/NF-κB pathway, subsequently diminishing MI-induced sympathetic neural remodeling and ventricular arrhythmias (VAs). PMID: 30721702 [PubMed - as supplied by publisher]
Source: European Journal of Pharmacology - February 2, 2019 Category: Drugs & Pharmacology Authors: Hu J, Huang CX, Rao PP, Zhou JP, Wang X, Tang L, Liu MX, Zhang GG Tags: Eur J Pharmacol Source Type: research