ArticleInternational journal of molecular sciences2026
Blocking MyD88 Signaling Pathway Protects Against Myocardial Ischemia Reperfusion by Inhibiting NOX/ROS Pathway and Enhancing eNOS Activity.
Article in International journal of molecular sciences, 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
Myocardial ischemia-reperfusion injury (MIRI) remains a major complication in acute coronary syndrome and cardiac surgery, with oxidative stress and metabolic dysregulation serving as central pathogenic drivers. This study aimed to clarify whether the novel MyD88 inhibitor TJ-M2010-5 confers cardioprotection against MIRI by remodeling immune-metabolic homeostasis, particularly through regulating NADPH oxidase (NOX)-derived reactive oxygen species (ROS) overproduction and endothelial nitric oxide synthase (eNOS) functional activity. In this study, male C57BL/6 mice were subjected to 30 min myocardial ischemia followed by 24 h reperfusion, with or without TJ-M2010-5 pretreatment (50 mg/kg, i.p.), and mouse cardiac vascular endothelial cells (H5V) were exposed to hypoxia-reoxygenation (H/R) with or without TJ-M2010-5 intervention. We systematically evaluated myocardial infarct size, ROS production, cell apoptosis, NF-κB activation, NOX expression and activity, NADPH redox homeostasis, NO production, and eNOS phosphorylation levels. The results showed that TJ-M2010-5 significantly reduced myocardial infarct size and inhibited IKKβ/NF-κB activation in I/R-treated mice, and functionally disrupted MyD88 homodimerization in ischemic myocardium. In H/R-challenged H5V cells, TJ-M2010-5 decreased ROS generation and cell apoptosis, suppressed NOX2/NOX4 expression and activity, restored NADPH levels and NADP
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