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Background Atrial fibrillation (AF) is the most common and progressive tachyarrhythmia. Diabetes is a common risk factor for AF. Recent research findings revealed that microtubule network disruption underlies AF.
View Article and Find Full Text PDFThe molecular role of Sigmar1 in regulating mitochondrial function through mitochondrial localization in cardiomyocytes.
Mitochondrion
January 2022
Department of Pathology and Translational Pathobiology, Louisiana State University Health Sciences Center-Shreveport, Shreveport, LA 71103, USA; Department of Molecular and Cellular Physiology, Louisiana State University Health Sciences Center-Shreveport, Shreveport, LA 71103, USA. Electronic address:
Sigmar1 is a widely expressed molecular chaperone protein in mammalian cell systems. Accumulating research demonstrated the cardioprotective roles of pharmacologic Sigmar1 activation by ligands in preclinical rodent models of cardiac injury. Extensive biochemical and immuno-electron microscopic research demonstrated Sigmar1's sub-cellular localization largely depends on cell and organ types.
View Article and Find Full Text PDFEndoplasmic Reticulum-Mitochondrial Contactology: Structure and Signaling Functions.
Trends Cell Biol
July 2018
MitoCare Center for Mitochondrial Imaging Research and Diagnostics, Department of Pathology, Anatomy and Cell Biology, Thomas Jefferson University, Philadelphia, PA 19107, USA. Electronic address:
Interorganellar contacts are increasingly recognized as central to the control of cellular behavior. These contacts, which typically involve a small fraction of the endomembrane surface, are local communication hubs that resemble synapses. We propose the term contactology to denote the analysis of interorganellar contacts.
View Article and Find Full Text PDFInositol 1,4,5-trisphosphate-mediated sarcoplasmic reticulum-mitochondrial crosstalk influences adenosine triphosphate production via mitochondrial Ca2+ uptake through the mitochondrial ryanodine receptor in cardiac myocytes.
Cardiovasc Res
October 2016
Department of Internal Medicine, Cardiology, University Hospital Würzburg, Oberdürrbacherstr. 6, 97080 Würzburg, Germany Comprehensive Heart Failure Center, University of Würzburg, Straubmühlweg 2a, 97078 Würzburg, Germany Medizinische Hochschule Brandenburg, Campus Klinikum Brandenburg/Havel, Abteilung für Kardiologie und Pneumologie, Hochstr. 29, 14770 Brandenburg an der Havel, Germany.
Aims: Elevated levels of inositol 1,4,5-trisphosphate (IP3) in adult cardiac myocytes are typically associated with the development of cardiac hypertrophy, arrhythmias, and heart failure. IP3 enhances intracellular Ca(2+ )release via IP3 receptors (IP3Rs) located at the sarcoplasmic reticulum (SR). We aimed to determine whether IP3-induced Ca(2+ )release affects mitochondrial function and determine the underlying mechanisms.
View Article and Find Full Text PDFPotential role of BNIP3 in cardiac remodeling, myocardial stiffness, and endoplasmic reticulum: mitochondrial calcium homeostasis in diastolic and systolic heart failure.
Circ Heart Fail
May 2013
Cardiovascular Institute, Mount Sinai School of Medicine, New York, NY, USA.
Background: We have shown that BNIP3 expression is significantly increased in heart failure (HF). In this study, we tested the effects of BNIP3 manipulation in HF.
Methods And Results: In a rat model of pressure overload HF, BNIP3 knockdown significantly decreased left ventricular (LV) volumes with significant improvement in LV diastolic and systolic function.
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