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Background: Loss of stromal interaction molecule 1 (STIM1) expression in smooth muscle cells protects against ischemia-reperfusion (I/R) injury. Whether and how decreased STIM1 expression in cardiomyocytes (CM) impacts cardiac remodeling in response to I/R injury remains unknown.
Objective: To examine mechanisms by which decreased CM-STIM1 expression in the adult heart modulates cardiac function before and after I/R injury.
Post-Myocardial Infarction (MI) Left Ventricular Free Wall Rupture Managed Conservatively.
Cureus
July 2024
Cardiology, Garden City Hospital, Garden City, USA.
Left ventricular free wall rupture (LVFWR) is an uncommon but often fatal complication of acute myocardial infarction. LVFWR is managed with hemodynamic stabilization and is typically followed by surgical intervention with varying approaches depending on the type of LVFWR. A 78-year-old male with a history of coronary artery bypass graft (CABG) was admitted with ST-segment elevation myocardial infarction.
View Article and Find Full Text PDFBiomaterial systems for evaluating the influence of ECM mechanics on anti-fibrotic therapeutic efficacy.
Matrix Biol Plus
August 2024
Joint Department of Biomedical Engineering of University of North Carolina, Chapel Hill and North Carolina State University, Raleigh, NC, 27695, USA.
Cardiac fibrosis is characterized by excessive accumulation and deposition of ECM proteins. Cardiac fibrosis is commonly implicated in a variety of cardiovascular diseases, including post-myocardial infarction (MI). We have previously developed a dual-delivery nanogel therapeutic to deliver tissue plasminogen activator (tPA) and Y-27632 (a ROCK inhibitor) to address MI-associated coronary artery occlusion and downregulate cell-contractility mediated fibrotic responses.
View Article and Find Full Text PDFChronic mitochondrial dynamic-targeted therapy alleviates left ventricular dysfunction by reducing multiple programmed cell death in post-myocardial infarction rats.
Eur J Pharmacol
August 2024
Cardiac Electrophysiology Research and Training Center, Faculty of Medicine, Chiang Mai University, Chiang Mai, 50200, Thailand; Cardiac Electrophysiology Unit, Department of Physiology, Faculty of Medicine, Chiang Mai University, Chiang Mai, 50200, Thailand; Center of Excellence in Cardiac Electrophysiology Research, Chiang Mai University, Chiang Mai, 50200, Thailand. Electronic address:
Mitochondrial dysfunction and the activation of multiple programmed cell death (PCD) have been shown to aggravate the severity and mortality associated with the progression of myocardial infarction (MI). Although pharmacological modulation of mitochondrial dynamics, including treatment with the fusion promoter (M1) and the fission inhibitor (Mdivi-1), exerted cardioprotection against several cardiac complications, their roles in the post-MI model have never been investigated. Using a MI rat model instigated by permanent left-anterior descending (LAD) coronary artery occlusion, post-MI rats were randomly assigned to receive one of 4 treatments (n = 10/group): vehicle (DMSO 3%V/V), enalapril (10 mg/kg), Mdivi-1 (1.
View Article and Find Full Text PDFMalonate given at reperfusion prevents post-myocardial infarction heart failure by decreasing ischemia/reperfusion injury.
Basic Res Cardiol
August 2024
Department of Medicine, University of Cambridge, Hills Road, Cambridge, CB2 0QQ, UK.
The mitochondrial metabolite succinate is a key driver of ischemia/reperfusion injury (IRI). Targeting succinate metabolism by inhibiting succinate dehydrogenase (SDH) upon reperfusion using malonate is an effective therapeutic strategy to achieve cardioprotection in the short term (< 24 h reperfusion) in mouse and pig in vivo myocardial infarction (MI) models. We aimed to assess whether inhibiting IRI with malonate given upon reperfusion could prevent post-MI heart failure (HF) assessed after 28 days.
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