ArticleBMC cardiovascular disorders2022
EGR2 is a hub-gene in myocardial infarction and aggravates inflammation and apoptosis in hypoxia-induced cardiomyocytes.
Article in BMC cardiovascular disorders, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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10 citing papers in PubMed, 17 citations in OpenAlex.
- EGR2 affects mixed stroke repair through BNIP3L-mediated microglial mitophagy.IBRO neuroscience reports · 2026Article
- Inhibition of Egr2 Protects against TAC-induced Heart Failure in Mice by Suppressing Inflammation and Apoptosis Via Targeting Acot1 in Cardiomyocytes.Journal of cardiovascular translational research · 2025Article
- CELF1 Promotes Post-myocardial Infarction Cardiac Remodeling Via Suppression of FMO2.Cardiovascular toxicology · 2025Article
- Multiple Signaling Axes (TNF-α/IL1β/IL8, TLR4/MYD88/NF-κB, and TGF-β1/ROS) Associated With Coronary Collateral Circulation of Coronary Chronic Total Occlusion in Geriatric Patients.Mediators of inflammation · 2025Article
- Bioinformatics analysis combined with untargeted metabolomics reveals lipid metabolism-related genes and their biological markers in chronic spontaneous urticaria.Frontiers in genetics · 2025Article
- Myocardial Matrix Hydrogels Mitigate Negative Remodeling and Improve Function in Right Heart Failure Model.JACC. Basic to translational science · 2024Article
- Application of biomedical materials in the diagnosis and treatment of myocardial infarction.Journal of nanobiotechnology · 2023Review
- LncRNAs and CircRNAs in Endoplasmic Reticulum Stress: A Promising Target for Cardiovascular Disease?International journal of molecular sciences · 2023Review
- Identification and verification of feature biomarkers associated in heart failure by bioinformatics analysis.Scientific reports · 2023Article
- Knockdown of GNL3L Alleviates the Progression of COPD Through Inhibiting the ATM/p53 Pathway.International journal of chronic obstructive pulmonary disease · 2023Article
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Authors and funding
9 authors at 6 institutions in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
backgroundMyocardial infarction (MI) is characterized by coronary artery occlusion, ischemia and hypoxia of myocardial cells, leading to irreversible myocardial damage. Therefore, it is urgent to explore the potential mechanism of myocardial injury during the MI process to develop effective therapies for myocardial cell rescue.
methodsWe downloaded the GSE71906 dataset from GEO DataSets, and the R software was used to identify the differentially expressed genes (DEGs) in mouse heart tissues of MI and sham controls. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment were performed to understand the significantly activated signaling pathways in MI. Protein-protein interaction (PPI) network was constructed to highlight the hub genes in DEGs. The Western Blot, qRT-PCR and TUNEL staining were used to explore the function of hub gene in hypoxia-induced cardiomyocytes in vitro.
resultsA total of 235 DEGs were identified in GSE71906 dataset. Functional enrichment analysis revealed that the upregulated genes were primarily associated with the inflammatory response and apoptosis. 20 hub genes were identified in PPI network, and the early growth response 2 (EGR2) was highlighted. In vitro. We confirmed the EGR2 was upregulated induced by hypoxia and revealed the upregulated EGR2 aggravates pro-inflammation and pro-apoptotic genes expression. In addition, EGR2 knockout mitigates hypoxia-induced inflammation and apoptosis in cardiomyocytes.
conclusionThe present study identified the EGR2 was a hub gene in myocardial damage during MI process, the excessive EGR2 aggravates hypoxia-induced myocardial damage by accelerating inflammation and apoptosis in vitro. Therefore, targeting EGR2 offers a potential pharmacological strategy for myocardial cell rescue in MI.
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