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Updated: Aug 25, 2025

Coronary Progenitor Cells and Soluble Biomarkers in Cardiovascular Prognosis after Coronary Angioplasty
Published on: January 28, 2020
The relationship between soluble lymphocyte activation gene-3 and coronary artery disease
Xinlin Xiong1, Zonggang Duan1, Haiyan Zhou1
1Department of Cardiology, The Affiliated Hospital of Guizhou Medical University, Guiyang, China.
Insights
Soluble lymphocyte activation gene 3 (sLAG3) levels are lower in coronary artery disease (CAD) patients and may indicate a novel risk factor for CAD development. Lower sLAG3 is associated with increased BMI and diabetes mellitus.
Area of Science:
- Immunology
- Cardiology
- Biochemistry
Background:
- Soluble lymphocyte activation gene 3 (sLAG3) is implicated in various diseases.
- The association between sLAG3 and coronary artery disease (CAD) remains unclear.
- Investigating sLAG3 in CAD is crucial for understanding disease mechanisms.
Purpose of the Study:
- To determine sLAG3 levels in CAD patients.
- To explore the clinical association of sLAG3 with CAD.
- To evaluate sLAG3 as a potential biomarker for CAD.
Main Methods:
- Enzyme-linked immunosorbent assay (ELISA) was used to measure sLAG3 levels.
- Clinical data, including demographics, biochemical markers, and coronary angiography, were collected.
- Gene expression data for LAG3 was analyzed from public datasets (GEO).
Main Results:
- sLAG3 levels were significantly lower in CAD patients compared to controls.
- Lower sLAG3 was negatively associated with CAD occurrence, BMI, and diabetes mellitus.
- LAG3 gene expression was downregulated in the peripheral blood of CAD patients.
Conclusions:
- Reduced sLAG3 levels are associated with CAD occurrence, not severity.
- sLAG3 may serve as a novel risk factor for developing CAD.
- sLAG3's association with BMI and diabetes highlights its potential role in metabolic-cardiac links.
Background:
Soluble lymphocyte activation gene 3 (sLAG3) may be used for diagnosis or prognosis in various diseases. However, the relationship between sLAG3 and coronary artery disease (CAD) are still unclear. This study aimed to investigate the levels of sLAG3 in patients with CAD, and its potential clinical association with the disease.
Methods:
A total of 66 subjects (49 patients with CAD and 17 control subjects without CAD) were enrolled. The sLAG3 level was measured using enzyme-linked immunosorbent assay (ELISA) kits. Clinical variables included demographics, biochemical markers, coronary angiography status, and ejection fraction of the heart (EF) were collected, and Gensini scores were calculated. LAG3 gene data was extracted from three datasets (GSE23561, GSE61144, GSE60993) in Gene Expression Omnibus (GEO) to compare differential expression between CAD and control subjects.
Results:
The sLAG3 level was significantly lower in the CAD vs. the controls (P < 0.05), and negatively associated with CAD [odds ratio (OR): 0.212, 95% confidential interval (CI): 0.060-0.746, P < 0.05]. Furthermore, the area under the curve (AUC) of sLAG3 level was significant (P < 0.05). The sLAG3 level in subjects with body mass index (BMI) ≥ 24 kg/m2 was lower compared to those with BMI < 24 kg/m2 (P < 0.05). The sLAG3 level was also negatively associated with BMI and diabetes mellitus (P < 0.05), though not associated with the Gensini scores or EF (P > 0.05). Lastly, the LAG3 gene expression in peripheral whole blood of patients with CAD were down-regulated compared to healthy controls (P < 0.05).
Conclusion:
The sLAG3 level was negatively associated with the occurrence but not severity of CAD. Meanwhile, the sLAG3 was negatively associated with BMI and diabetes mellitus, suggesting the reduced sLAG3 might be a novel risk factor for developing CAD.
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