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http://dx.doi.org/10.1097/INF.0b013e31823058dd | DOI Listing |
Circ Cardiovasc Qual Outcomes
January 2025
Division of Cardiovascular Medicine, Department of Internal Medicine, Lahey Hospital and Medical Center, Burlington, MA (S.S.D.).
BMJ Open
December 2024
Institute for Cardio-Metabolic Medicine, University Hospital Coventry & Warwickshire NHS Trust, University of Warwick Medical School and Coventry University, Coventry, UK
Objective: To estimate the resource use of patients with obstructive hypertrophic cardiomyopathy (HCM), stratified by New York Heart Association (NYHA) class, in the English and Northern Irish healthcare systems via expert elicitation.
Design: Modified Delphi framework methodology.
Setting: UK HCM secondary care centres (n=24).
Am J Physiol Heart Circ Physiol
January 2025
Department of Biochemistry and Molecular Biology, Dalhousie University, Dalhousie Medicine New Brunswick, 355 Campus Ring Road, Saint John, New Brunswick, E2L 4L5, Canada.
Lipid phosphate phosphatase 3 (LPP3) is a membrane-bound enzyme that hydrolyzes lipid phosphates including the bioactive lipid, lysophosphatidic acid (LPA). Elevated circulating LPA production and cellular LPA signaling are implicated in obesity-induced metabolic and cardiac dysfunction. Deletion of LPP3 in the cardiomyocyte increases circulating LPA levels and causes heart failure and mitochondrial dysfunction in mice.
View Article and Find Full Text PDFJ Mol Cell Cardiol Plus
June 2024
Division of Pulmonary Circulation, Department of Cardiovascular Medicine, National Cerebral and Cardiovascular Center, Suita, Osaka, Japan.
Background: Pulmonary hypertension (PH) often leads to right ventricle (RV) failure, a significant cause of morbidity and mortality. Despite advancements in PH management, progression to RV maladaptation and subsequent failure remain a clinical challenge. This study explored the effect of paroxetine, a selective serotonin reuptake inhibitor (SSRI), on RV function in a rat model of PH, hypothesizing that it improves RV function by inhibiting G protein-coupled receptor kinase 2 (GRK2) and altering myofilament protein phosphorylation.
View Article and Find Full Text PDFBiophys J
January 2025
Department of Biological Sciences & Center for Biotechnology and Interdisciplinary Studies, Rensselaer Polytechnic Institute Troy, NY 12180, USA; Department of Biomedical Engineering, Center for Biotechnology and Interdisciplinary Studies, Rensselaer Polytechnic Institute Troy, NY 12180, USA. Electronic address:
Stretch activation (SA), a delayed increase in force production following rapid muscle lengthening, is critical to the function of vertebrate cardiac muscle and insect asynchronous indirect flight muscle (IFM). SA enables or increases power generation in muscle types used in a cyclical manner. Recently, myosin isoform expression has been implicated as a mechanism for varying the amplitude of SA in some muscle types.
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