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Sci Rep
January 2025
Department of Cardiology, Angiology and Pneumology, University Hospital Heidelberg, Heidelberg, Germany.
Pathological cardiac remodeling is a maladaptive response that leads to changes in the size, structure, and function of the heart. These changes occur due to an acute or chronic stress on the heart and involve a complex interplay of hemodynamic, neurohormonal and molecular factors. As a critical regulator of cell growth, protein synthesis and autophagy mechanistic target of rapamycin complex 1 (mTORC1) is an important mediator of pathological cardiac remodeling.
View Article and Find Full Text PDFZhonghua Yi Xue Za Zhi
January 2025
Ningbo Hangzhou Bay Hospital(Ningbo Branch of Renji Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai),Ningbo315336, China.
To develop a predictive model for improvement of ejection fraction 1 year after heart failure with reduced ejection fraction (HFrEF) following acute ST-segment elevation myocardial infarction (STEMI). This nested case-control study included STEMI patients diagnosed with HFrEF from a prospective multicenter multimodality imaging cohort between August 2014 and March 2021. Based on the improvement of left ventricular ejection fraction (LVEF) at baseline and 1-year follow-up, the patients were classified into the heart failure with improved ejection fraction (HFimpEF) group and the persistent HFrEF group.
View Article and Find Full Text PDFAnal Chim Acta
February 2025
Department of Chemistry, University of Waterloo, Waterloo, ON, Canada. Electronic address:
Background: Normothermic ex situ heart perfusion (ESHP) has emerged as a valid modality for advanced cardiac allograft preservation and conditioning prior to transplantation though myocardial function declines gradually during ESHP thus limiting its potential for expanding the donor pool. Recently, the utilization of dialysis has been shown to preserve myocardial and coronary vasomotor function. Herein, we sought to determine the changes in myocardial metabolism that could support this improvement.
View Article and Find Full Text PDFBiochem Biophys Res Commun
January 2025
Cardiovascular Research Group, Department of Pharmacy, COMSATS University Islamabad, Abbottabad Campus, University Road, Tobe Camp, Abbottabad, 22060, KPK, Pakistan. Electronic address:
Gentisic acid (GA), a cytochrome P450 metabolite of the antiplatelet drug aspirin, exhibits smooth muscle relaxant, antiatherogenic, and antioxidant activities. It also has a protective role in hypertrophic heart failure, suggesting its role in the management of myocardial infarction (MI). This study aimed to explore the protective activity of GA in isoproterenol (ISO)-induced MI in Sprague-Dawley (SD) rats in-vivo, followed by mechanistic investigation ex-vivo.
View Article and Find Full Text PDFFront Biosci (Landmark Ed)
January 2025
Department of Cardiology, Affiliated Hospital of Jiangnan University, 214122 Wuxi, Jiangsu, China.
Background: Myocardial ischemia-reperfusion (I/R) injury refers to cell damage that occurs as a consequence of the restoration of blood circulation following reperfusion therapy for cardiovascular diseases, and it is a primary cause of myocardial infarction. The search for nove therapeutic targets in the context of I/R injury is currently a highly active area of research. p70 ribosomal S6 kinase (S6K1) plays an important role in I/R induced necrosis, although the specific mechanisms remain unclear.
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