ORIGINAL RESEARCH article
Front. Endocrinol.
Sec. Cardiovascular Endocrinology
Volume 16 - 2025 | doi: 10.3389/fendo.2025.1539646
This article is part of the Research TopicRenal Dysfunction in Cardiometabolic Disease: Implications of Inflammation and Oxidative StressView all 4 articles
Comprehensive Bioinformatics Analysis and Experimental Verification Identify Mitochondrial Gene Dgat2 as A Novel Therapeutic Biomarker for Myocardial Ischemia-Reperfusion
Provisionally accepted- 1Xijing Hospital, Air Force Medical University, Xi’an, Shaanxi Province, China
- 2Xi'an Jiaotong University, Xi'an, China
Select one of your emails
You have multiple emails registered with Frontiers:
Notify me on publication
Please enter your email address:
If you already have an account, please login
You don't have a Frontiers account ? You can register here
Background: Ischemic cardiomyopathy is a severe disease marked by high morbidity and mortality, often exacerbated by myocardial ischemia/reperfusion injury (MI/RI). Mitochondrial metabolism plays a critical role in MI/RI progression. This study aimed to identify potential new targets and biomarkers for mitochondria-related genes in MI/RI. Methods: MI/R microarray data (GSE160516) from the GEO database and a mitochondrial geneset were analyzed. Limma identified differentially expressed genes (DEGs), followed by GSEA, GO, and KEGG pathway enrichment. Mitochondria-related DEGs (MitoDEGs) were pinpointed. Protein-Protein Interaction (PPI) networks and machine learning identified key MitoDEGs. Regulatory networks were constructed using transcription factor (TF) predictions.Immune cell infiltration was assessed with ImmuCelAl, and correlations between MitoDEGs and immune cell levels were examined. Mouse myocardial ischemia-reperfusion models were established to validate pivotal MitoDEGs.Results: MitoDEGs were enriched in bio-oxidation, immune-inflammation, and oxidative stress pathways. Machine learning identified two hub genes: Dgat2 and Cybb. Dgat2 was significantly elevated in ischemia-reperfusion mouse models, confirmed by RT-PCR and Western blot.Functional enrichment indicated that Dgat2 may be involved in biological oxidation and lipid metabolism. TF prediction suggested PPARG as a regulator of Dgat2 expression. Immune infiltration analysis revealed significant correlations between Dgat2 and immune cells, including CD4_T_cells and NK cells, suggesting a role for immunity in MI/RI.We found that Dgat2 could be exploited as a novel mitochondria-related gene target and biomarker in myocardial ischemia-reperfusion injury, which is of great clinical significance.
Keywords: Myocardial ischemia/reperfusion injury, Mitochondria, DGAT2, Bioinformatics analysis, Oxidative Stress
Received: 04 Dec 2024; Accepted: 09 May 2025.
Copyright: © 2025 Li, Zhou, Xue, Yin, Liu, Wu, Zhao, An and Sun. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
* Correspondence: Yang Sun, Xijing Hospital, Air Force Medical University, Xi’an, Shaanxi Province, China
Disclaimer: All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers. Any product that may be evaluated in this article or claim that may be made by its manufacturer is not guaranteed or endorsed by the publisher.