Shahid Bahonar University of Kerman and Iranian Biotechnology Society Agricultural Biotechnology Journal 2228-6705 18 3 2026 08 23 S100A1 downregulation as a calcium-energetic marker in acute myocardial infarction: Correlation with angiogenic and inflammatory pathways S100A1 downregulation as a calcium-energetic marker in acute myocardial infarction: Correlation with angiogenic and inflammatory pathways 251 268 5413 10.22103/jab.2026.26901.1859 FA Elham F. Hamzah College of Medicine, Babylon University, Hillah, Iraq 0009-0001-8944-2563 Abdulsamie Hassan Altaee College of Medicine, Babylon University, Hillah, Iraq. 0000-0002-2951-7973 Ameer Aljubawii College of Medicine, Babylon University, Hillah, Iraq 0000-0002-9801-6929 Journal Article 2026 02 23 ObjectiveAcute myocardial infarction (AMI) is a condition of synchronized biological reprogramming characterized by calcium dysregulation, inflammatory activation, and compromised vascular repair. S100A1 is a Ca²⁺-binding protein abundant in cardiomyocytes that is crucial for excitation-contraction coupling and mitochondrial energetics, thus potentially indicating cardiac functional stability beyond necrotic damage. The aim of this study was to assess S100A1 protein and its mRNA expression, as well as their correlation with inflammatory and vascular mediators in patients with AMI. Materials and methodsThis case-control study (n = 176) assessed circulating S100A1 protein and gene expression in conjunction with TNF-α and VEGF-A levels. Venous blood samples (5 mL) were obtained from patients with acute myocardial infarction (AMI) within 12 hours of symptoms onset and from control participants at the time of enrolment. Quantitative real-time polymerase chain reaction (qPCR) was conducted with SYBR Green dye and the Stratagene Mx3005P platform. Statistical analyses were conducted utilizing SPSS (IBM v25.0) and GraphPad Prism (v9.0). ResultsPatients with acute myocardial infarction showed a marked decrease in S100A1 protein levels, both at the protein level and at the transcriptional level, compared to healthy patients. This decrease was concurrent with a decrease in VEGF-A levels and an increase in TNF-α levels. TNF-α and VEGF-A were shown to be significantly positively correlated (r = 0.396, p = 0.013; *p < 0.05). The expression of S100A1 showed no discernible linear correlation with inflammatory mediators, indicating that the calcium-energetic axis is rather independent. Quantitative real-time PCR analysis revealed a significant downregulation of S100A1 mRNA expression in patients with (AMI) compared with healthy controls. The mean ΔCt difference was approximately 2.1 cycles (95% CI: 1.95-2.25), indicating an estimated 4.3-fold decrease in S100A1 protein mRNA expression in acute myocardial infarction.Conclusion Thus, these results support the inclusion of S100A1 in multi-marker frameworks to enhance risk classification in acute myocardial infarction and highlight its significance as a mechanistic biomarker for compromised cardiac function. ObjectiveAcute myocardial infarction (AMI) is a condition of synchronized biological reprogramming characterized by calcium dysregulation, inflammatory activation, and compromised vascular repair. S100A1 is a Ca²⁺-binding protein abundant in cardiomyocytes that is crucial for excitation-contraction coupling and mitochondrial energetics, thus potentially indicating cardiac functional stability beyond necrotic damage. The aim of this study was to assess S100A1 protein and its mRNA expression, as well as their correlation with inflammatory and vascular mediators in patients with AMI. Materials and methodsThis case-control study (n = 176) assessed circulating S100A1 protein and gene expression in conjunction with TNF-α and VEGF-A levels. Venous blood samples (5 mL) were obtained from patients with acute myocardial infarction (AMI) within 12 hours of symptoms onset and from control participants at the time of enrolment. Quantitative real-time polymerase chain reaction (qPCR) was conducted with SYBR Green dye and the Stratagene Mx3005P platform. Statistical analyses were conducted utilizing SPSS (IBM v25.0) and GraphPad Prism (v9.0). ResultsPatients with acute myocardial infarction showed a marked decrease in S100A1 protein levels, both at the protein level and at the transcriptional level, compared to healthy patients. This decrease was concurrent with a decrease in VEGF-A levels and an increase in TNF-α levels. TNF-α and VEGF-A were shown to be significantly positively correlated (r = 0.396, p = 0.013; *p < 0.05). The expression of S100A1 showed no discernible linear correlation with inflammatory mediators, indicating that the calcium-energetic axis is rather independent. Quantitative real-time PCR analysis revealed a significant downregulation of S100A1 mRNA expression in patients with (AMI) compared with healthy controls. The mean ΔCt difference was approximately 2.1 cycles (95% CI: 1.95-2.25), indicating an estimated 4.3-fold decrease in S100A1 protein mRNA expression in acute myocardial infarction.Conclusion Thus, these results support the inclusion of S100A1 in multi-marker frameworks to enhance risk classification in acute myocardial infarction and highlight its significance as a mechanistic biomarker for compromised cardiac function. https://jab.uk.ac.ir/article_5413_ddb1b62e0c8c0b8b020fb2a35cee6494.pdf