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Novel Mouse Model of Myocardial Infarction, Plaque Rupture, and Stroke Shows Improved Survival With Myeloperoxidase Inhibition.
Circulation
August 2024
Robert M. Berne Cardiovascular Research Center (S. Shamsuzzaman, R.A.D., A.S., V.S., V.M.M., S.K. S. Saibaba, L.S.S., G.K.O.), University of Virginia School of Medicine, Charlottesville.
Background: Thromboembolic events, including myocardial infarction (MI) or stroke, caused by the rupture or erosion of unstable atherosclerotic plaques are the leading cause of death worldwide. Although most mouse models of atherosclerosis develop lesions in the aorta and carotid arteries, they do not develop advanced coronary artery lesions. Moreover, they do not undergo spontaneous plaque rupture with MI and stroke or do so at such a low frequency that they are not viable experimental models to study late-stage thrombotic events or to identify novel therapeutic approaches for treating atherosclerotic disease.
View Article and Find Full Text PDFThe troponin trap: a deep dive into incorporation and feedback sanction biases in NSTEMI diagnoses.
Acta Cardiol
September 2024
Cardiology, Instituto Dante Pazzanese de Cardiologia, São Paulo, Brasil.
Postoperative myocardial injury and platelet reactivity in patients undergoing vascular surgery: The platelet reactivity and postoperative myocardial injury after major vascular surgery (PROMISE) study.
Thromb Res
October 2022
Department of Anaesthesiology, Intensive Care and Pain Medicine, St. Antonius Hospital, Nieuwegein, the Netherlands; Department of Anaesthesiology, Intensive Care and Pain Medicine, University Medical Centre, Utrecht, the Netherlands. Electronic address:
Background: Postoperative myocardial injury (PMI) after major vascular surgery, detected by elevated cardiac troponin (cTn), has been associated with morbidity and mortality. It is unclear whether the pathophysiology of PMI is determined by increased platelet activity.
Objective: To examine the relationship between platelet activation (P-selectin expression) and PMI in patients undergoing elective open abdominal aortic surgery.
Modulation of cardiac thin filament structure by phosphorylated troponin-I analyzed by protein-protein docking and molecular dynamics simulation.
Arch Biochem Biophys
August 2022
Department of Physiology & Biophysics, Boston University School of Medicine, 700 Albany Street, Boston, MA, 02118, USA. Electronic address:
Tropomyosin, controlled by troponin-linked Ca-binding, regulates muscle contraction by a macromolecular scale steric-mechanism that governs myosin-crossbridge-actin interactions. At low-Ca, C-terminal domains of troponin-I (TnI) trap tropomyosin in a position on thin filaments that interferes with myosin-binding, thus causing muscle relaxation. Steric inhibition is reversed at high-Ca when TnI releases from F-actin-tropomyosin as Ca and the TnI switch-peptide bind to the N-lobe of troponin-C (TnC).
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