ArticlePeerJ2026
Integrated transcriptomic and metabolomic analysis reveals the regulatory role of itaconic acid in inflammatory infiltration during myocardial ischemia-reperfusion injury.
Article in PeerJ, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Background: Inflammatory infiltration constitutes a fundamental pathophysiological mechanism in myocardial ischemia-reperfusion (IR) injury, characterized by its role in initiating tissue damage, amplifying pathological inflammatory cascades, and exacerbating structural and functional impairment of the myocardium. Integrated transcriptomic and metabolomic analysis identified the metabolite itaconic acid as a potential key regulator in IR injury. Therefore, we assessed the effect of its derivative, 4-octyl itaconate (4-OI), on inflammatory infiltration in a mouse model of IR injury. Methods: Following establishment of a myocardial IR model, tissue samples from the infarct border zone were harvested for transcriptomics and wide-target metabolomic sequencing. Bioinformatics methods were used to analyze the transcriptomics and metabolomics results separately and to perform a joint analysis. Molecular docking and molecular dynamics modeling were employed to explore proteins bound to itaconic acid. Following intragastric administration of 4-OI to myocardial IR mice, echocardiography was performed. Plasma levels of interleukin-4 (IL4), interleukin10 (IL10), cardiac troponin T (cTnT), and creatine kinase-myocardial band (CKMB) were measured by enzyme-linked immunosorbent assay (ELISA). Myocardial inflammatory infiltration was evaluated by hematoxylin and eosin Staining (HE staining), while inflammatory marker expression associated with macrophages was evaluated by immunohistochemical staining for inducible nitric oxide synthase (iNOS) and immune responsive gene 1 (IRG1). Macrophage heterogeneity was further assessed by immunofluorescence co-localization staining for F4/80, CCR2, and CD206. Additionally, mRNA expression levels of Interleukin-1 beta (Il1b), Tumor Necrosis Factor-alpha (Tnfa), Il4, and Il10 in myocardial tissue were quantified by quantitative reverse transcription polymerase chain reaction (qRT-PCR). Results: Integrated transcriptomic and metabolomic analysis identified itaconic acid as a potential metabolite modulating myocardial IR injury. Preliminary molecular docking analysis suggested possible
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