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http://dx.doi.org/10.1038/nature10493 | DOI Listing |
Background: This study investigates the effects of intranasal dantrolene nanoparticles on inflammation and programmed cell death by pyroptosis in 5XFAD Alzheimer's Disease (AD) mice.
Methods: 5XFAD and wild type (WT) B6SJLF1/J mice were treated with intranasal dantrolene nanoparticles (5 mg/kg), daily, Monday to Friday, for 12 weeks continuously, starting at 9 months of age. Blood and brain were harvested at 13 months of age, one month after completion of 12 weeks intranasal dantrolene nanoparticle treatment.
bioRxiv
December 2024
Department of Anesthesiology and Critical Care, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104, U.S.A.
J Physiol
April 2024
Department of Cell and Molecular Physiology, Stritch School of Medicine, Loyola University Chicago, Maywood, IL, USA.
Calcium release from the endoplasmic reticulum (ER) is predominantly driven by two key ion channel receptors, inositol 1, 4, 5-triphosphate receptor (InsPR) in non-excitable cells and ryanodine receptor (RyR) in excitable and muscle-based cells. These calcium transients can be modified by other less-studied ion channels, including polycystin 2 (PC2), a member of the transient receptor potential (TRP) family. PC2 is found in various cell types and is evolutionarily conserved with paralogues ranging from single-cell organisms to yeasts and mammals.
View Article and Find Full Text PDFJ Mol Cell Cardiol
June 2023
KU Leuven, Department of Cardiovascular Sciences, Laboratory of Experimental Cardiology, 3000 Leuven, Belgium. Electronic address:
Basic Res Cardiol
November 2022
Department of Cardiovascular Sciences, Laboratory of Experimental Cardiology, KU Leuven, 3000, Leuven, Belgium.
Dysregulated intracellular Ca handling involving altered Ca release from intracellular stores via RyR channels underlies both arrhythmias and reduced function in heart failure (HF). Mechanisms linking RyR dysregulation and disease are not fully established. Studies in animals support a role for InsP receptor Ca channels (InsPR) in pathological alterations in cardiomyocyte Ca handling but whether these findings translate to the divergent physiology of human cardiomyocytes during heart failure is not determined.
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