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Indoxyl Sulfate Induces Ventricular Arrhythmias Attenuated by Secretoneurin in Right Ventricular Outflow Tract Cardiomyocytes.
Cardiovasc Toxicol
January 2025
Graduate Institute of Clinical Medicine, College of Medicine, Taipei Medical University, No. 250, Wuxing St., Taipei, 11031, Taiwan.
Ventricular arrhythmias (VAs) are major causes of sudden cardiac death in chronic kidney disease (CKD) patients. Indoxyl sulfate (IS) is one common uremic toxin found in CKD patients. This study investigated whether IS could induce VAs via increasing right ventricular outflow tract (RVOT) arrhythmogenesis.
View Article and Find Full Text PDFConstitutive deletion of the obscurin-Ig58/59 domains induces atrial remodeling and Ca2+-based arrhythmogenesis.
JCI Insight
January 2025
Department of Biochemistry and Molecular Biology, University of Maryland School of Medicine, Baltimore, United States of America.
Obscurin is a giant protein that coordinates diverse aspects of striated muscle physiology. Obscurin immunoglobulin domains 58/59 (Ig58/59) associate with essential sarcomeric and Ca2+ cycling proteins. To explore the pathophysiological significance of Ig58/59, we generated the Obscn-ΔIg58/59 mouse model, expressing obscurin constitutively lacking Ig58/59.
View Article and Find Full Text PDFLeft superior cervical ganglia lymph node mimicry and its role in rat ventricular arrhythmias following myocardial infarction.
Acta Physiol (Oxf)
February 2025
Department of Cardiology, Cheeloo College of Medicine, Shandong Provincial Qianfoshan Hospital, Shandong University, Jinan, China.
Aim: Sympathetic overactivation may lead to severe ventricular arrhythmias (VAs) post-myocardial infarction (MI). The superior cervical ganglion (SCG) is an extracardiac sympathetic ganglion which regulates cardiac autonomic tone. We aimed to investigate the characteristics and functional significance of SCG on neuro-cardiac communication post-MI.
View Article and Find Full Text PDFInterleukin-1β Drives Disease Progression in Arrhythmogenic Cardiomyopathy.
bioRxiv
December 2024
Department of Biomedical Sciences, Florida State University College of Medicine; Tallahassee, FL, USA.
Arrhythmogenic cardiomyopathy (ACM) is a genetic form of heart failure that affects 1 in 5000 people globally and is caused by mutations in cardiac desmosomal proteins including , and . Individuals with ACM suffer from ventricular arrhythmias, sudden cardiac death, and heart failure. There are few effective treatments and heart transplantation remains the best option for many affected individuals.
View Article and Find Full Text PDFInteractions between the developing heart and the embryonic immune system are essential for proper cardiac development and maintaining homeostasis, with disruptions linked to various diseases. While human pluripotent stem cell (hPSC)-derived organoids are valuable models for studying human organ function, they often lack critical tissue-resident immune cells. Here, we introduce an advanced human heart assembloid model, termed hHMA (human heart-macrophage assembloid), which fully integrates autologous cardiac tissue- resident macrophages (MPs) with pre-existing human heart organoids (hHOs).
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