{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,7,30]],"date-time":"2026-07-30T22:19:12Z","timestamp":1785449952189,"version":"3.56.0"},"reference-count":31,"publisher":"Frontiers Media SA","license":[{"start":{"date-parts":[[2025,9,25]],"date-time":"2025-09-25T00:00:00Z","timestamp":1758758400000},"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. Cardiovasc. Med."],"abstract":"<jats:sec><jats:title>Background<\/jats:title><jats:p>Acute myocardial infarction (AMI) is a leading cause of cardiovascular mortality and perioperative complications in the elderly (&amp;gt;65 years). However, existing clinical biomarkers (e.g., troponin) still lack sufficient sensitivity for ultra-early diagnosis. A comprehensive understanding of the dynamic changes in serum biomarkers post-AMI is crucial for developing novel diagnostic strategies.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p>A rat AMI model was established by surgical ligation of the left anterior descending (LAD) coronary artery. Cardiac function was evaluated via echocardiography and triphenyltetrazolium chloride (TTC) staining at 24\u2005h post-AMI. Blood samples were collected at baseline (pre-anesthesia) and at 1, 2, 6, 12, 24, and 48\u2005h post-LAD ligation. Serum levels of 25 biomarkers were measured by ELISA, including: \u03b1-smooth muscle actin (\u03b1-SMA), aminopeptidase N (ANPEP), B-type natriuretic peptide (BNP), C-C chemokine receptor type 2 (CCR2), C-reactive protein (CRP), connective tissue growth factor (CTGF), C-X-C motif chemokine ligand 16 (CXCL16), cystatin C (Cys), dopamine D2 receptor (D2D), glucagon-like peptide-1 (GLP-1), homocysteine (Hcy), chemokine-like factor 1 (CKLF1), high-sensitivity troponin I (hs-TnI), interleukin-1\u03b2 (IL-1\u03b2), interleukin-6 (IL-6), lipoprotein(a) (Lp-\u03b1), monocyte chemoattractant protein-1 (MCP-1), matrix metalloproteinase-9 (MMP-9), NOD-like receptor family pyrin domain-containing 3 (NLRP3), plasminogen activator inhibitor-1 (PAI-1), S100 calcium-binding protein A8 (S100A8), solute carrier family 31 member 1 (copper transporter, SLC31A1), tissue inhibitor of metalloproteinases-1 (TIMP-1), tumor necrosis factor-\u03b1 (TNF-\u03b1), and vascular endothelial growth factor A (VEGF-A).<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>At 24\u2005h post-AMI, LVEF was significantly decreased in the AMI group (63.84\u2009\u00b1\u20092.48% vs. 38.83\u2009\u00b1\u20092.62%, <jats:italic>p<\/jats:italic>\u2009&amp;lt;\u20090.001), with an infarct size of 28.70\u2009\u00b1\u20091.43%. A total of 25 blood biomarkers potentially associated with AMI were detected. Among them, 17 biomarkers showed rapid elevation within 1\u2005h post-AMI (excluding IL-6, TNF-\u03b1, ANPEP, D2D, CXCL16, Lp-\u03b1 and \u03b1-SMA). IL-6, TNF-\u03b1 and ANPEP exhibited significant elevation at 2\u2005h post-AMI, while CXCL16 showed obvious elevation at 6\u2005h and \u03b1-SMA demonstrated significant elevation at 12\u2005h. However, S100A8, GLP-1, MMP-9 and NLRP3 showed a decrease at 2\u2005h, although their overall trend within 48\u2005h was upward. Lp-\u03b1 and D2D remained below baseline levels throughout the observation period, with both showing levels below baseline at 1\u2005h post-AMI. They returned to baseline levels at 12\u2005h and 2\u2005h respectively, followed by rapid decreases again<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusion<\/jats:title><jats:p>This study is the first to systematically characterize the dynamic profiles of 25 serum biomarkers following AMI in rats, revealing that: (1) IL-1\u03b2, S100A8, BNP, SLC31A1 and Cys may serve as an ultra-early (1\u2005h) diagnostic panel (increase of over 70% at 1\u2005h); (2) the delayed elevation of \u03b1-SMA and CXCL16 may be associated with the initiation of myocardial repair; (3) the suppression of Lp-\u03b1 and D2D might reflect compensatory protective mechanisms.<\/jats:p><\/jats:sec>","DOI":"10.3389\/fcvm.2025.1631648","type":"journal-article","created":{"date-parts":[[2025,9,25]],"date-time":"2025-09-25T05:30:12Z","timestamp":1758778212000},"update-policy":"https:\/\/doi.org\/10.3389\/crossmark-policy","source":"Crossref","is-referenced-by-count":2,"title":["Dynamic profiles of 25 serum 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