{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,7,2]],"date-time":"2026-07-02T02:45:34Z","timestamp":1782960334341,"version":"3.54.5"},"reference-count":39,"publisher":"Frontiers Media SA","license":[{"start":{"date-parts":[[2026,7,2]],"date-time":"2026-07-02T00:00:00Z","timestamp":1782950400000},"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. Genet."],"abstract":"<jats:sec>\n                    <jats:title>Background<\/jats:title>\n                    <jats:p>Acute myocardial infarction (AMI), a highly fatal cardiovascular emergency, presents ongoing clinical challenges in both early diagnosis and the elucidation of its associated immuno-inflammatory processes. By integrating multi-omics data, this research seeks to identify novel diagnostic biomarkers and uncover their potential mechanisms in AMI.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>\n                      By integrating transcriptomic data, core genes linked to AMI were identified by differential expression and weighted gene co-expression network analysis (WGCNA). A multivariate logistic regression diagnostic model was constructed based on these genes, and its diagnostic efficacy was evaluated with receiver operating characteristic (ROC) curve analysis.\n                      <jats:italic>In vitro<\/jats:italic>\n                      , an oxygen-glucose deprivation\/reperfusion (OGD\/R) model was generated in AC16 human cardiomyocytes. We used lentiviral transduction to knock down the key gene. Cell proliferation was evaluated by Cell Counting Kit-8 (CCK-8) assay, apoptosis levels were measured by Terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) staining and flow cytometry, and the mRNA and protein expression of key genes were detected with qRT-PCR and Western blot.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      Three AMI core genes (PLA2G15, ADAP2, and FAM20C) were successfully identified. The diagnostic model established via multifactorial logistic regression exhibited satisfactory discriminatory power.\n                      <jats:italic>In vitro<\/jats:italic>\n                      experiments confirmed that ADAP2 expression was markedly upregulated in the OGD\/R model. Knocking down ADAP2 effectively alleviated OGD\/R-induced suppression of cell proliferation, apoptosis enhancement, and expression increase of inflammatory factors (TNF-\u03b1, IL-6, IL-1\u03b2). Mechanistically, ADAP2 knockdown inhibited the expression of key proteins in the IL-17 signaling pathway (IL-17A, IL-17RA, ACT1). Exogenous addition of rhIL-17A reversed the protective effect of ADAP2 knockdown against cellular injury.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion<\/jats:title>\n                    <jats:p>The combined diagnostic model derived from the AMI core genes PLA2G15, ADAP2, and FAM20C exhibited robust diagnostic power for noninvasive diagnosis. ADAP2 can influence AMI-induced myocardial injury through the IL-17 signaling pathway.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.3389\/fgene.2026.1828693","type":"journal-article","created":{"date-parts":[[2026,7,2]],"date-time":"2026-07-02T02:13:26Z","timestamp":1782958406000},"update-policy":"https:\/\/doi.org\/10.3389\/crossmark-policy","source":"Crossref","is-referenced-by-count":0,"title":["Application of acute myocardial infarction-related key genes in noninvasive diagnosis: a comprehensive analysis based on transcriptome and single-cell transcriptome"],"prefix":"10.3389","volume":"17","author":[{"given":"Mingbin","family":"Xie","sequence":"first","affiliation":[{"name":"Department of Cardiology, Hangzhou Red Cross Hospital","place":["Hangzhou, Zhejiang, China"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yuanhong","family":"Wu","sequence":"additional","affiliation":[{"name":"Department of Cardiology, Hangzhou Red Cross Hospital","place":["Hangzhou, Zhejiang, China"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Xinyao","family":"Jin","sequence":"additional","affiliation":[{"name":"Department of Cardiology, Hangzhou Red Cross Hospital","place":["Hangzhou, Zhejiang, China"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Fengchun","family":"Jiang","sequence":"additional","affiliation":[{"name":"Department of Cardiology, Hangzhou Red Cross Hospital","place":["Hangzhou, Zhejiang, China"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Qiang","family":"Yao","sequence":"additional","affiliation":[{"name":"Department of Cardiology, Hangzhou Red Cross Hospital","place":["Hangzhou, Zhejiang, China"]}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"1965","published-online":{"date-parts":[[2026,7,2]]},"reference":[{"key":"B1","doi-asserted-by":"publisher","first-page":"357","DOI":"10.1016\/j.tcm.2022.02.005","article-title":"Myocardial ischemia-reperfusion injury and the influence of inflammation","volume":"33","author":"Algoet","year":"2023","journal-title":"Trends Cardiovasc Med."},{"key":"B2","doi-asserted-by":"publisher","first-page":"7588","DOI":"10.3390\/ijms26157588","article-title":"ArfGAP with dual pleckstrin homology domains 2 promotes hypertrophy of cultured neonatal cardiomyocytes","volume":"26","author":"Berthiaume","year":"2025","journal-title":"Int. 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