Background: Circular RNAs (circRNAs) are involved in the progression of atherosclerosis (AS). The present study aimed to determine the functions and mechanism of circ_0003575 in AS.
Methods: Oxidized low-density lipoprotein (ox-LDL) was used to induce human aortic endothelial cells (HAECs) to establish an AS cell model.
Objective: The prognostic factors of young patients aged ≤40 years with ST-segment elevation myocardial infarction (STEMI) remain unclear. This study explored risk factors that may affect the 1-year prognosis of young STEMI patients by analyzing patient data of baseline, clinical regimen, and secondary prevention.
Methods: Baseline and clinical data were collected from 420 STEMI patients aged ≤40 years.
In this study, we intend to explore the potential function of l-ascorbic acid in hypoxia-reoxygenation (H/R)-induced damage of CMECs and its related molecular mechanism. With different concentrations of l-ascorbic acid treatment, the proliferation, migration, inflammation and autophagy of cardiac microvascular endothelial cells (CMECs) were determined by several biological experiments. Si-HMGB1 transfection was used to reduce HMGB1 expression and to detect the function of HMGB1 in H/R-induced damage of CMECs.
View Article and Find Full Text PDFObjective: To investigate the role of miR-362-3p and its target in cardiomyocytes with hypoxia/reoxygenation (H/R) injury.
Results: We found that miR-362-3p was decreased in myocardial infarction (MI) samples, and promoted the proliferation and restrained the apoptosis of H/R-injured H9c2 cells. TP53INP2 was recognized as the target of miR-362-3p and negatively modulated by miR-362-3p.
Objective: To observe the efficacy and safety of dopamine plus furosemide in treating patients with heart failure.
Methods: This research included 150 patients with heart failure who were diagnosed and treated at our hospital between March 2018 and November 2020. The patients were randomly assigned to a study group or a reference group according to the data of admission (the cut-off date was June 2019).
This study aimed to explore the function of miR-24 in hypoxia/reoxygenation (H/R) -induced cardiomyocyte injury.We constructed a cardiomyocyte model of H/R using the primary cardiomyocytes isolated from Sprague-Dawley rats. To explore the role of miR-24, cells were transfected with a miR-24 mimic or miR-24 inhibitor.
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