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血清S100A12在脓毒症诱导的心肌功能障碍临床诊断中的应用:生物信息学与临床数据分析整合研究

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

作者信息

Wu Fang, Hong Helin, Tian Ye, Wang Xiaoyan

机构信息

Department of Emergency, The First People's Hospital of Guiyang, Guiyang, China.

出版信息

Front Cardiovasc Med. 2025 Aug 25;12:1640788. doi: 10.3389/fcvm.2025.1640788. eCollection 2025.

DOI:10.3389/fcvm.2025.1640788
PMID:40926894
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC12415004/
Abstract

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.

摘要

目的

脓毒症是重症监护病房中常见的危及生命的综合征,常伴有心肌功能障碍,这会显著恶化患者的预后。S100A12是一种与炎症相关的钙结合蛋白,在各种炎症状态下表达上调。然而,其在脓毒症及相关心脏损伤中的作用仍不清楚。

方法

本研究使用来自基因表达综合数据库(GEO)的数据集进行差异表达分析,以评估脓毒症和脓毒症诱导的心肌功能障碍(SIMD)中S100A12表达的变化,随后进行基因本体(GO)和京都基因与基因组百科全书(KEGG)通路富集分析。将诊断为脓毒症的患者分为SIMD组和非SIMD组,同时设置健康对照组。通过酶联免疫吸附测定(ELISA)和逆转录定量聚合酶链反应(RT-qPCR)评估血清S100A12的表达。评估其与心肌酶、炎症标志物和心功能指标的相关性。

结果

生物信息学分析显示脓毒症和SIMD中S100A12表达上调,富集于多个与炎症相关的通路。临床上,SIMD组中S100A12的mRNA和蛋白水平较高。S100A12浓度与心肌肌钙蛋白I(cTnI)、肌酸激酶同工酶(CK-MB)、降钙素原(PCT)和白细胞介素-6(IL-6)呈正相关,而与平均动脉压(MAP)和左心室射血分数(LVEF)呈负相关。逻辑回归确定S100A12是SIMD的独立危险因素。

结论

作为一种炎症生物标志物,S100A12具有独立的预测价值,其与心肌酶的联合应用有助于建立有效的临床预警模型。该研究突出了一个潜在的新生物标志物和治疗靶点,可能有助于脓毒症相关心脏损伤的早期检测和管理。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a102/12415004/267ce4ca8be4/fcvm-12-1640788-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a102/12415004/f0fc8e0c55cd/fcvm-12-1640788-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a102/12415004/18c3843932de/fcvm-12-1640788-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a102/12415004/4edd14672aa6/fcvm-12-1640788-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a102/12415004/5a989f3728ca/fcvm-12-1640788-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a102/12415004/9c0ad9c01aaf/fcvm-12-1640788-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a102/12415004/267ce4ca8be4/fcvm-12-1640788-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a102/12415004/f0fc8e0c55cd/fcvm-12-1640788-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a102/12415004/18c3843932de/fcvm-12-1640788-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a102/12415004/4edd14672aa6/fcvm-12-1640788-g003.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a102/12415004/267ce4ca8be4/fcvm-12-1640788-g006.jpg

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Sci Rep. 2025 May 8;15(1):15975. doi: 10.1038/s41598-025-00829-2.
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Association between S100A12 and risk of peripheral arterial disease in patients with dyslipidemia: a cross-sectional study.S100A12与血脂异常患者外周动脉疾病风险的关联:一项横断面研究。
BMC Cardiovasc Disord. 2025 Apr 24;25(1):313. doi: 10.1186/s12872-025-04752-2.
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Inhibition of S100A12 Attenuates LPS-Induced Endothelial Barrier Dysfunction in HPMECs through the JAK2/STAT3 Signaling Pathway.
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Curr Mol Med. 2025 Apr 17. doi: 10.2174/0115665240338945250317082242.
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Metabolic Biomarkers Mediate Allergic Conjunctivitis via Circulating Inflammatory Proteins: Evidence From a Mendelian Randomization Study.代谢生物标志物通过循环炎症蛋白介导过敏性结膜炎:孟德尔随机化研究的证据
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