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MicroRNA-34a (miR-34a) is expressed in the myocardium and expression is altered after myocardial injury. We investigated the effects of miR-34a on heart function after ischemia-reperfusion (IR) injury. Cardiomyocytes were isolated from neonatal rat hearts and simulated IR injury was induced in vitro. Following IR injury in rats, infarct size was measured and left ventricular (LV) function was evaluated using echocardiography. Protein expression of silent information regulator 1 (SIRT1), acetylated p53 (ac-p53), Bcl-2 and Bax, and miR-34a and SIRT1 gene levels were analyzed. miR-34a overexpression exacerbated myocardial injury by increasing apoptosis and infarct size and decreasing LV function. Suppression of miR-34a attenuated myocardial IR injury. SIRT1 was negatively regulated by miR-34a and the expression of downstream genes, such as ac-p53, Bcl-2, and Bax were altered correspondingly. Increased expression of miR-34a aggravates injury after IR; miR-34a suppression therapy may represent a new line of treatment for myocardial IR injury.
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http://dx.doi.org/10.1089/scd.2017.0062 | DOI Listing |
Front Cardiovasc Med
August 2025
Department of Emergency, The First People's Hospital of Guiyang, Guiyang, China.
Objective: Sepsis is a common and life-threatening syndrome in intensive care units, frequently accompanied by myocardial dysfunction, which significantly worsens patient outcomes. S100A12, a calcium-binding protein associated with inflammation, is upregulated in various inflammatory conditions. However, its role in sepsis and related cardiac injury remains unclear.
View Article and Find Full Text PDFAm J Chin Med
September 2025
Department of Pharmacology.
Notoginsenoside R1 (NGR1), a natural triterpenoid saponin, is extracted from , and has cardiovascular and cerebrovascular protective effects due to anti-inflammatory, anti-oxidant, and anti-apoptotic properties. Previous research has suggested a protective role for NGR1 in myocardial ischemia/reperfusion (MI/R) injury. However, the potential mechanisms involved have not been fully elucidated.
View Article and Find Full Text PDFMed Eng Phys
October 2025
Departament of Electronics and Biomedical Engineering, School of Electrical and Computer Engineering (DEEB/FEEC), University of Campinas (UNICAMP), Campinas, SP, Brazil; National Laboratory for Study of Cell Calcium (LabNECC), Center for Biomedical Engineering (CEB), UNICAMP, Campinas, SP, Brazil.
High-intensity, external electric fields (HIEF) have been used in research and therapy for abnormal generation/propagation of the cardiac electrical activity (e.g., defibrillation), and for promoting access of membrane-impermeant molecules into the cytosol through electropores.
View Article and Find Full Text PDFEuropace
September 2025
Department of Cardiology and Vascular Medicine, University Heart and Vascular Center Frankfurt, Goethe University Frankfurt, Frankfurt am Main, Germany.
Background And Aims: Aim of this study was to assess the risk of hemolysis, the extent of myocardial and neural injury after monopolar, monophasic pulsed field ablation (PFA) using a lattice-tip catheter in comparison to single-shot PF ablation platforms employing bipolar, biphasic waveforms.
Methods: This prospective study included consecutive patients undergoing PFA for atrial fibrillation (AF) using the Affera™ mapping and ablation system (n=40). Biomarkers for hemolysis (haptoglobin, LDH, bilirubin), myocardial injury (high-sensitive troponin T, CK, CK-MB), neurocardiac injury (S100), and renal function (creatinine) were assessed pre- and within 24 hours post-ablation.
Pediatr Infect Dis J
September 2025
From the Department of Pediatric Intensive Care Unit, The Affiliated Hospital of Qingdao University, Qingdao, Shandong, China.
Background: Antiviral drugs and coronavirus disease 2019 (COVID-19) vaccines have significantly reduced COVID-19-related hospitalizations and deaths in infected children. However, COVID-19 continues to pose a major mortality risk in young children. High-sensitive cardiac troponin (Hs-cTn) is a specific marker of myocardial cell damage.
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