Serum S100A12 in the clinical diagnosis of sepsis-induced myocardial dysfunction: an integrated bioinformatics and clinical data analysis.

Objective: Sepsis is a common and life-threatening syndrome in intensive care units, frequently accompanied by myocardial dysfunction, which significantly worsens patient outcomes. S100A12, a calcium-binding protein associated with inflammation, is upregulated in various inflammatory conditions. However, its role in sepsis and related cardiac injury remains unclear. Methods: This study performed differential expression analysis using datasets from GEO to evaluate changes in S100A12 expression in sepsis and sepsis-induced myocardial dysfunction (SIMD), followed by GO and KEGG pathway enrichment analyses. Patients diagnosed with sepsis were assigned into SIMD and non-SIMD groups, along with healthy controls. Serum S100A12 expression was evaluated by ELISA and RT-qPCR. Correlations with cardiac enzymes, inflammatory markers, and cardiac function indicators were assessed. Results: Bioinformatics analysis showed upregulation of S100A12 in sepsis and SIMD, enriched in multiple inflammation-related pathways. Clinically, S100A12 mRNA and protein levels were higher in the SIMD group. There was a positive association between S100A12 concentrations and cTnI, CK-MB, PCT, and IL-6, whereas MAP and LVEF exhibited a negative correlation. Logistic regression identified S100A12 as an independent risk factor for SIMD. Conclusion: As an inflammatory biomarker, S100A12 has independent predictive value, and its combination with cardiac enzymes enables the development of an efficient clinical warning model. The study highlights a potential new biomarker and treatment focus that could aid in early detection and management of sepsis-related cardiac injury.