AI Networking Cookbook: Practical recipes for AI-assisted network automation and development
TL;DR
Hypoxia/reoxygenation assays using H9C2 rat cardiomyocytes confirmed the upregulation of Myc and Rnf115 during early MIRI, aligning with bioinformatics trends.
This study aimed to screen and identify core hypoxia‐ischemia‐related genes associated with myocardial infarction (MI).
This integrated computational and experimental study identifies a set of high-value diagnostic core genes in AMI and validates the specific upregulation of novel genes (GPR97, PROK2) in myocardial ischemia, placing them within a pathological network involving metabolic, immune and protective pathways.
In vivo, miR-221-3p antagomir pre-treatment restored CPT2, reduced reactive oxygen species (ROS) and NET-associated markers, lowered apparent infarct burden, and improved acute cardiac function, and identified 18 metabolites associated with IHD after false-discovery-rate (FDR) correction.
The regulatory network of HF-MI is mapped, suggesting potential involvement of the GLIS3-HCP5 and ZNF135-PVT1 axes in HF-MI, thereby providing a basis for exploring novel therapeutic strategies.
In vivo qPCR results verified that the mRNA expression of CEBPB and PPP1R15A was significantly elevated in myocardial tissues of AMI model mice compared with the sham group, and have high research potential for exploring the molecular mechanism of myocardial ischemic injury.
The findings suggest that CCL4 may serve as a potential diagnostic biomarker for AMI, and the observed immune-metabolic associations provide a basis for future mechanistic and translational studies.
We use cookies to run the site and, with your consent, for analytics and to show ads. See our Cookie Policy.