Key result
Elevated SOCS3 gene expression was higher in AMI patients compared to SCAD patients (1.33-fold higher mRNA, 1.25-fold higher protein; p<0.05) and was an independent risk factor for AMI.
Why the study?
It was unknown whether suppressor of cytokine signaling 3 (SOCS3) gene expression could serve as a biomarker to predict the risk of acute myocardial infarction.
Is elevated expression of the SOCS3 gene associated with an increased risk of acute myocardial infarction?
Case-Control (n=205)
Is elevated expression of the SOCS3 gene associated with an increased risk of acute myocardial infarction?
Effect estimate: 1.33-fold higher mRNA and 1.25-fold higher protein
p-value: p=< 0.05
Elevated SOCS3 gene expression in peripheral white blood cells is an independent risk factor for acute myocardial infarction.
May support SOCS3 as AMI biomarker; hypothesis-generating and requires prospective validation before clinical use.
Aims: The present study was designed to evaluate whether the expression of the suppressor of cytokine signaling 3 (SOCS3) gene could serve as a biomarker to predict the risk of acute myocardial infarction (AMI). Basic Methods: Peripheral white blood cells were collected from 113 patients with AMI and 92 patients with stable coronary artery disease (SCAD). SOCS3 mRNA expression levels in peripheral blood cells were determined by a real-time quantitative polymerase chain reaction, and levels of the SOCS3 protein were determined by Western blotting. Results: The mRNA expression levels of the SOCS3 gene in AMI patients was 1.33-fold higher than that in the SCAD patients, and the level of the SOCS3 protein was 1.25-fold higher (p < 0.05 for both). Bivariate logistic regression analysis documented that elevated expression of the SOCS3 gene was an independent risk factor for AMI. A regression analysis demonstrated a lack of correlation between elevated expression levels of SOCS3 and the levels of fasting blood glucose high- and low-density lipoprotein, and cardiac troponin. Conclusions: Elevated expression of the SOCS3 gene results most likely from enhanced inflammatory responses and is an independent risk factor for AMI.
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Meng et al. (2020) conducted a case-control in Acute Myocardial Infarction (n=205). Elevated SOCS3 gene expression vs. Stable coronary artery disease (SCAD) was evaluated on SOCS3 mRNA and protein expression levels (1.33-fold higher mRNA and 1.25-fold higher protein, p=< 0.05). Elevated SOCS3 gene expression was higher in AMI patients compared to SCAD patients (1.33-fold higher mRNA, 1.25-fold higher protein; p<0.05) and was an independent risk factor for AMI.
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