Expression Pattern and Molecular Mechanism of Oxidative Stress-Related Genes in Myocardial Ischemia–Reperfusion Injury

Wu, Jiahe; Luo, Jingyi; Cai, Huanhuan; Li, Chenze; Lei, Zhe; Lu, Yi; Ni, Lihua; Cao, Jinxin; Cheng, Bolin; Hu, Xiaorong

doi:10.3390/jcdd10020079

Cited by 2 publications

(1 citation statement)

References 51 publications

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“…Gene Ontology (GO) annotation and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analysis were completed with the “cluster Profiler package” of R software (version 4.0.1) ( 20 , 21 ). GO analysis includes three parts: biological process (BP) analysis, cellular component (CC) analysis, and molecular function (MF) analysis.…”

Section: Methodsmentioning

confidence: 99%

Transcriptomic analysis reveals the lipid metabolism-related gene regulatory characteristics and potential therapeutic agents for myocardial ischemia-reperfusion injury

Wu,

Cai,

et al. 2024

Front. Cardiovasc. Med.

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BackgroundImpaired energy balance caused by lipid metabolism dysregulation is an essential mechanism of myocardial ischemia-reperfusion injury (MI/RI). This study aims to explore the lipid metabolism-related gene (LMRG) expression patterns in MI/RI and to find potential therapeutic agents.MethodsDifferential expression analysis was performed to screen the differentially expressed genes (DEGs) and LMRGs in the MI/RI-related dataset GSE61592. Enrichment and protein-protein interaction (PPI) analyses were performed to identify the key signaling pathways and genes. The expression trends of key LMRGs were validated by external datasets GSE160516 and GSE4105. The corresponding online databases predicted miRNAs, transcription factors (TFs), and potential therapeutic agents targeting key LMRGs. Finally, the identified LMRGs were confirmed in the H9C2 cell hypoxia-reoxygenation (H/R) model and the mouse MI/RI model.ResultsEnrichment analysis suggested that the “lipid metabolic process” was one of the critical pathways in MI/RI. Further differential expression analysis and PPI analysis identified 120 differentially expressed LMRGs and 15 key LMRGs. 126 miRNAs, 55 TFs, and 51 therapeutic agents were identified targeting these key LMRGs. Lastly, the expression trends of Acadm, Acadvl, and Suclg1 were confirmed by the external datasets, the H/R model and the MI/RI model.ConclusionAcadm, Acadvl, and Suclg1 may be the key genes involved in the MI/RI-related lipid metabolism dysregulation; and acting upon these factors may serve as a potential therapeutic strategy.

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Section: Methodsmentioning

confidence: 99%

Transcriptomic analysis reveals the lipid metabolism-related gene regulatory characteristics and potential therapeutic agents for myocardial ischemia-reperfusion injury

Wu,

Cai,

et al. 2024

Front. Cardiovasc. Med.

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N-acetylcysteine Protects Against Myocardial Ischemia–Reperfusion Injury Through Anti-ferroptosis in Type 1 Diabetic Mice

Zhou,

Yang,

Chen

et al. 2024

Cardiovasc Toxicol

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The hearts of subjects with diabetes are vulnerable to ischemia–reperfusion injury (IRI). In contrast, experimentally rodent hearts have been shown to be more resistant to IRI at the very early stages of diabetes induction than the heart of the non-diabetic control mice, and the mechanism is largely unclear. Ferroptosis has recently been shown to play an important role in myocardial IRI including that in diabetes, while the specific mechanisms are still unclear. Non-diabetic control (NC) and streptozotocin-induced diabetic (DM) mice were treated with the antioxidant N-acetylcysteine (NAC) in drinking water for 4 week starting at 1 week after diabetes induction. Mice were subjected to myocardial IRI induced by occluding the coronary artery for 30 min followed by 2 h of reperfusion, subsequently at 1, 2, and 5 week of diabetes induction. The post-ischemic myocardial infarct size in the DM mice was smaller than that in NC mice at 1 week of diabetes but greater than that in the NC mice at 2 and 5 week of diabetes, which were associated with a significant increase of ferroptosis at 2 and 5 week but a significant reduction of ferroptosis at 1 week of diabetes. NAC significantly attenuated post-ischemic ferroptosis as well as oxidative stress and reduced infarct size at 2 and 5 week of diabetes. Application of erastin, a ferroptosis inducer, reversed the cardioprotective effects of NAC. It is concluded that increased oxidative stress and ferroptosis are the major factors attributable to the increased vulnerability to myocardial IRI in diabetes and that attenuation of ferroptosis represents a major mechanism whereby NAC confers cardioprotection against myocardial IRI in diabetes.

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Expression Pattern and Molecular Mechanism of Oxidative Stress-Related Genes in Myocardial Ischemia–Reperfusion Injury

Cited by 2 publications

References 51 publications

Transcriptomic analysis reveals the lipid metabolism-related gene regulatory characteristics and potential therapeutic agents for myocardial ischemia-reperfusion injury

Transcriptomic analysis reveals the lipid metabolism-related gene regulatory characteristics and potential therapeutic agents for myocardial ischemia-reperfusion injury

N-acetylcysteine Protects Against Myocardial Ischemia–Reperfusion Injury Through Anti-ferroptosis in Type 1 Diabetic Mice

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