Key result
Hongqi Shenmai Decoction improves post-MI cardiac function and reduces injury by inhibiting EGFR/JAK2-STAT3 signaling.
Why the study?
Post-MI heart failure is driven by adverse ventricular remodeling and mitochondrial dysfunction, but the upstream regulation of cardiolipin in failing myocardium and the role of EGFR/JAK2-STAT3 signaling remain unclear.
Does Hongqi Shenmai Decoction ameliorate post-myocardial infarction heart failure in preclinical models?
Does Hongqi Shenmai Decoction ameliorate post-myocardial infarction heart failure in preclinical models?
Hongqi Shenmai Decoction demonstrates cardioprotective effects in preclinical post-myocardial infarction heart failure models by preserving mitochondrial cardiolipin homeostasis through the attenuation of EGFR/JAK2-STAT3 signaling.
BACKGROUND Post-myocardial infarction heart failure (post-MI HF) is driven by adverse ventricular remodeling and mitochondrial dysfunction. Cardiolipin is essential for mitochondrial integrity, but its upstream regulation in failing myocardium remains unclear. Whether Hongqi Shenmai Decoction (HQSMD) preserves cardiolipin homeostasis through epidermal growth factor receptor (EGFR)/Janus kinase 2 (JAK2)-signal transducer and activator of transcription 3 (STAT3) signaling has not been defined. PURPOSE To determine whether HQSMD alleviates post-MI HF by preserving cardiolipin-related metabolic homeostasis through modulation of the EGFR/JAK2-STAT3 pathway. STUDY DESIGN An in vivo post-MI HF mouse model and an in vitro oxygen-glucose deprivation/reoxygenation (OGD/R)-injured AC16 cardiomyocyte model were integrated with chemical profiling, multi-omics analysis, target validation, and epidermal growth factor (EGF)-mediated rescue experiments. METHODS Cardiac function, infarct injury, fibrosis, oxidative stress, mitochondrial ultrastructure, and mitochondrial function were assessed. Ultra-performance liquid chromatography-mass spectrometry, transcriptomics, untargeted metabolomics, molecular docking, surface plasmon resonance, western blotting, immunofluorescence, and cardiolipin-related functional assays were performed. RESULTS HQSMD improved cardiac function and attenuated infarction, remodeling, oxidative stress, and mitochondrial injury in post-MI HF mice. Multi-omics analyses implicated EGFR/JAK-STAT signaling and cardiolipin-related glycerophospholipid disturbances. HQSMD suppressed MI- or OGD/R-induced phosphorylation of EGFR, JAK2, and STAT3 Tyr705 while preserving mitochondrial STAT3/Ser727 signaling. In cardiomyocytes, HQSMD reduced apoptosis and restored mitochondrial dynamics, biogenesis, redox balance, membrane potential, mPTP function, cardiolipin-associated fluorescence, and cardiolipin-related enzyme expression. EGF partially reversed these effects. CONCLUSION HQSMD protects against post-MI HF mainly by attenuating pathological EGFR/JAK2-dependent STAT3 Tyr705 activation, thereby preserving cardiolipin-related metabolic homeostasis and mitochondrial integrity.
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Bo et al. (2026) studied Post-myocardial infarction heart failure. Hongqi Shenmai Decoction was evaluated on Cardiac function, infarct injury, fibrosis, oxidative stress, and mitochondrial function. Hongqi Shenmai Decoction improved cardiac function and attenuated infarction and mitochondrial injury in post-MI mice and cardiomyocytes by suppressing pathological EGFR/JAK2-STAT3 signaling.
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