Coronary artery disease (CAD) is one of the main causes of hospitalization worldwide and has high morbidity. MicroRNAs (miRNAs) play an important role in the pathogenesis of cardiovascular diseases. miR-451 is a special miRNA that is involved in many cancers' development. At present, there is no research about miR-451 in coronary heart disease. In this study, we aimed to identify the action mechanism of miR-451 in coronary heart disease and human umbilical vein endothelial cells (HUVECs). In this study, we found that miR-451 is up-regulated in the peripheral blood of patients with coronary heart disease. Moreover, TargetScan and dual-luciferase reporter gene assay results showed that VEGFA is a direct target gene of miR-451. C (CCK-8) and flow cytometry assay results showed that miR-451 mimic significantly inhibits cell proliferation and promotes apoptosis in HUVECs. Moreover, we found that the role of miR-451 in HUVECs is associated with the PI3K-Akt-mTOR pathway. Taken together, the data indicates that miR-451 might be a novel bio-marker for coronary heart disease.
Download full-text PDF |
Source |
---|---|
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6944456 | PMC |
http://dx.doi.org/10.1515/med-2020-0001 | DOI Listing |
J Burn Care Res
January 2025
Department of Rehabilitation Medicine, Hangang Sacred Heart Hospital, College of Medicine, Hallym University, Seoul, Korea.
Septic arthritis (SA) are rare in patients with burns, but delayed treatment can result in irreversible joint destruction. Early diagnosis and immediate treatment are necessary to prevent joint destruction. Robot training in patients with musculoskeletal diseases and burns, can improve joint range of motion (ROM), muscle strength, and lower extremity function.
View Article and Find Full Text PDFHypertension
January 2025
Department of Nephrology, Medical Faculty, University Hospital Düsseldorf, Heinrich Heine University Düsseldorf, Germany (S.A.P., I.Q., D. Arifaj, M.K., D. Argov, L.C.R., J.S.).
Background: Ciliary neurotrophic factor (CNTF), mainly known for its neuroprotective properties, belongs to the IL-6 (interleukin-6) cytokine family. In contrast to IL-6, the effects of CNTF on the vasculature have not been explored. Here, we examined the role of CNTF in AngII (angiotensin II)-induced hypertension.
View Article and Find Full Text PDFCirc Genom Precis Med
January 2025
Centre for Heart Lung Innovation, University of British Columbia, Vancouver. (K.H., M.A., L.R., Y.L., A.S., H.H., L.R.B., Z.W.L.).
Background: Protein-truncating mutations in the titin gene are associated with increased risk of atrial fibrillation. However, little is known about the underlying pathophysiology.
Methods: We identified a heterozygous titin truncating variant (TTNtv) in a patient with unexplained early onset atrial fibrillation and normal ventricular function.
Circ Cardiovasc Interv
January 2025
Centre for Cardiovascular Innovation, University of British Columbia, Vancouver, Canada. (A.H., J.J., S.O., K.M., J.A.L., P.B., D.A.W., S.L.S., J.G.W., J.S.).
Background: Transcatheter heart valve (THV) underexpansion after transcatheter aortic valve replacement may be associated with worse outcomes. THV expansion can be assessed fluoroscopically using a pigtail for calibration; however, the accuracy of this technique specific to transcatheter aortic valve replacement is unknown. We assessed the accuracy and reproducibility of a novel fluoroscopic method to assess THV expansion using the THV commissural post for calibration.
View Article and Find Full Text PDFCirc Arrhythm Electrophysiol
January 2025
Biosense Webster, Inc, Irvine, CA (J.M., T.S., S.F.-H.).
Background: Sequential application of radiofrequency with pulsed field (PF) ablation may increase lesion depth while preserving the advantages of PF. The study's aim was to determine lesion dimensions of sequential, colocalized radiofrequency and PF ablation.
Methods: A preclinical study using swine (n=4) performed lesions in the right/left ventricles.
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!