Acute myocardial infarction (MI), a critical and dangerous manifestation of coronary heart disease caused by arterial thrombosis or bypass thrombosis, rapidly leads to myocardial ischemia and hypoxia, ending in heart failure.
PANoptosis, an inflammation-dependent, inflammatory form of programmed cell death, involves a complex molecular network in which pyroptosis, apoptosis, and necroptosis cooperatively mediate apoptotic programs. However, the causal relationships and regulatory mechanisms linking MI and PANoptosis are not yet clear. Furthermore, DNA methylation regulates PANoptosis pathways, thereby mediating changes in heart disease.
Genome-wide association studies (GWAS) and summary data-based Mendelian randomization (SMR) are novel methods for identifying potential causal targets by integrating expression quantitative trait loci (eQTL) and methylation quantitative trait loci (mQTL)]. GWAS data for MI were integrated with protein quantitative trait loci (pQTL) data for plasma proteins to obtain therapeutic plasma protein targets.
Methylation regulatory sites in MI were identified by integrating eQTL and mQTL data, and pathogenic genes in MI were identified by examining neutrophil invagination, eQTL, MI GWAS data, and transcriptomic databases. However, no studies have been conducted to date on DNA methylation and pathogenic genes related to PANoptosis, the central mechanism of MI. The aim of this study was to investigate potential therapeutic targets and regulatory mechanisms of PANoptosis genes in the pathogenesis of MI, with a focus on DNA methylation modulation.
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Kun Zhou, Yingjiu Jiang, and Jiajie Leng. Potential therapeutic targets of PANoptosis in myocardial infarction: A summary data-based Mendelian randomization study integrating eQTL, mQTL, and multi-GWAS data. CVIA. 2025. Vol. 10(1). DOI: 10.15212/CVIA.2024.0072
