{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,4]],"date-time":"2026-08-04T15:02:38Z","timestamp":1785855758305,"version":"3.56.0"},"reference-count":67,"publisher":"Frontiers Media SA","license":[{"start":{"date-parts":[[2026,2,17]],"date-time":"2026-02-17T00:00:00Z","timestamp":1771286400000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":["frontiersin.org"],"crossmark-restriction":true},"short-container-title":["Front. Immunol."],"abstract":"\n Background<\/jats:title>\n Acute myocardial infarction (AMI) is a global health burden. Ferroptosis drives cardiomyocyte death, but specific ferroptosis-related genes (FRGs) and pathways underlying ischemic injury remain unclear.<\/jats:p>\n <\/jats:sec>\n \n Methods<\/jats:title>\n First, differentially expressed mRNAs (DE-mRNAs) from GSE61144 were intersected with FRGs to obtain differentially expressed ferroptosis-related genes (DE-FRGs). Subsequently, GO\/KEGG functional enrichment, PPI network construction, expression heatmap visualization and tissue-specific expression were performed on DE-FRGs to clarify their biological characteristics. To explore the potential causal relationship between DE-FRGs and AMI, we conducted summary-data-based Mendelian randomization (SMR) analysis in four cardiovascular-related tissues and performed Bayesian colocalization analysis, ultimately identifying a key transcription factor (TF). With this TF as the hub, a miRNA-TF-mRNA regulatory network was constructed. Based on this pathway, we conducted a series of analyses, including prediction of transcription factor binding sites, GSEA and GeneMANIA analysis, prediction of gene-diseases and gene-drugs associations, phenome-wide association study (PheWAS), ROC curve assessment and RT-qPCR validation, thereby systematically elucidating the molecular mechanisms of this pathway in AMI.<\/jats:p>\n <\/jats:sec>\n \n Results<\/jats:title>\n \n The SMR analysis showed that one key TF-\n SP1<\/jats:italic>\n were significantly associated with AMI risk among the four types of tissues [coronary artery, atrial appendage, left ventricle and whole blood (\n p<\/jats:italic>\n SMR &lt; 0.05,\n p<\/jats:italic>\n HEIDI &gt; 0.05, OR &gt; 1)] in the GTEx database. Bayesian colocalization analysis indicated a strong colocalization relationship between\n SP1<\/jats:italic>\n and AMI (PPH4\u2009=\u20090.81). Using\n SP1<\/jats:italic>\n as the key TF, a miRNA-TF-mRNA network was constructed, including 132 mRNAs and 358 miRNAs. Further narrow down to 2 miRNAs (miR-327 and miR-133b) and 7 mRNAs (\n EGR1<\/jats:italic>\n ,\n IL6<\/jats:italic>\n ,\n MYC<\/jats:italic>\n ,\n NR4A1<\/jats:italic>\n ,\n P4HA1<\/jats:italic>\n ,\n PLAUR<\/jats:italic>\n and\n VEGFA<\/jats:italic>\n ) through validated by the GSE76604 and GSE4648 datasets. Bayesian colocalization analysis further confirmed that\n PLAUR<\/jats:italic>\n is the key mRNA and has a strong colocalization relationship with AMI (PPH4\u2009=\u20090.99). Ultimately, we successfully established the miR-133b\/\n SP1<\/jats:italic>\n \/\n PLAUR<\/jats:italic>\n -ferroptosis signaling pathway. Further analyses provided additional validation for the possibility of\n SP1<\/jats:italic>\n and miR-133b\/\n SP1<\/jats:italic>\n \/\n PLAUR<\/jats:italic>\n axis as a prognostic marker and therapeutic target in AMI.\n <\/jats:p>\n <\/jats:sec>\n \n Conclusions<\/jats:title>\n \n In this study, by integrating transcriptomic, SMR and PheWAS analysis, we first established a robust causal association between\n SP1<\/jats:italic>\n and AMI risk across four cardiovascular tissues, and subsequently delineated a miR-133b\/\n SP1<\/jats:italic>\n \/\n PLAUR<\/jats:italic>\n ferroptosis pathway in AMI.\n <\/jats:p>\n <\/jats:sec>","DOI":"10.3389\/fimmu.2026.1742618","type":"journal-article","created":{"date-parts":[[2026,2,17]],"date-time":"2026-02-17T05:18:41Z","timestamp":1771305521000},"update-policy":"https:\/\/doi.org\/10.3389\/crossmark-policy","source":"Crossref","is-referenced-by-count":1,"title":["Potential of SP1 as a prognostic marker and therapeutic target in acute myocardial 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