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Methylation-modified genes regulating macrophage polarization through signaling pathways to mediate sepsis-induced myocardial cell injury
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DOI：10.1080/08923973.2026.2673959.png)
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Abstract
En 中文
Sepsis is a systemic inflammatory response caused by infection, often accompanied by myocardial injury. Studies have shown that methylation modifications are associated with immune cell polarization, but their role in sepsis-induced myocardial injury remains unclear. This article aimed to investigate how methylation modifications regulate macrophage polarization through the phosphoinositide 3-kinase/protein kinase B/mammalian target of Rapamycin (PI3K/AKT/mTOR) signaling pathway, thereby influencing sepsis-induced myocardial injury.
Sepsis was induced by lipopolysaccharide (LPS), and interventions included methylation inhibition, PI3K inhibition, and Interleukin-10 (IL-10) overexpression. Myocardial injury and immune responses were assessed by measuring physiological indicators, myocardial injury markers, hematoxylin-eosin (HE) staining, immunohistochemistry, and immunological assays in rats.
After sepsis induction, myocardial injury was more pronounced in the methylation inhibition and PI3K inhibition groups, while the IL-10 overexpression group exhibited milder injury. Immunological assays showed that the proportion of M1 macrophages was increased in the methylation and PI3K inhibition groups, while the IL-10 overexpression group maintained a higher proportion of M2 macrophages.
Methylation modifications could regulate macrophage polarization through PI3K-related signaling pathways, thereby aggravating sepsis-induced myocardial injury.IL-10, by promoting M2 macrophage function, attenuates myocardial injury and holds potential therapeutic value.
Keywords:
Macrophage polarization
methylation modifications
myocardial injury
PI3K/AKT/mTOR signaling pathway
sepsis
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