Key result
TLR2 expression was significantly upregulated in patients with myocardial infarction compared to healthy controls, with a standardized mean difference of 2.55 and an AUC of 0.76.
Why the study?
The clinical implication of TLR2 in myocardial infarction remains contradictory, and its molecular mechanism is still unknown.
Meta-Analysis (n=631)
Standardized Mean Difference: 2.55 (95% CI 1.35–3.75)
TLR2 is significantly upregulated in myocardial infarction, suggesting a potential role in disease progression and value as a screening biomarker.
TLR2 may aid myocardial infarction screening; leaves open its clinical utility pending prospective validation.
OBJECTIVE: The prevalence and mortality of cardiovascular diseases remain ranked first worldwide. Myocardial infarction (MI) is the central cause of death from cardiovascular diseases, seriously endangering human health. The clinical implication of toll-like receptor 2 (TLR2) remains contradictory, and its mechanism is still unknown. Hence, the objective of this study was to elucidate the clinical value and molecular mechanism of TLR2 in MI. METHODS: All high-throughput datasets and eligible literature were screened, and the expression levels of TLR2 were collected from the MI. The integrated expression level of TLR2 was displayed by calculating the standardized mean difference (SMD) and the area under the curve (AUC) of the summary receiver operating characteristic curve (sROC). The related TLR2 genes were sent for pathway analyses by gene ontology (GO), Kyoto encyclopedia of genes and genome (KEGG), and disease ontology (DO). Single-cell RNA-seq was applied to ascertain the molecular mechanism of TLR2 in MI. RESULTS: Nine microarrays and four reported data were available to calculate the comprehensive expression level of TLR2 in MI, including 325 cases of MI and 306 cases of controls. The SMD was 2.55 (95% CI = 1.35-3.75), and the AUC was 0.76 (95% CI = 0.72-0.79), indicating the upregulation of TLR2 in MI. The related TLR2 genes were primarily enriched in the pathways of atherosclerosis, arteriosclerotic cardiovascular disease, and arteriosclerosis, suggesting the clinical role of TLR2 in the progression of MI. Afterward, TLR2 was upregulated in myeloid cells in MI. CONCLUSIONS: TLR2 may have a crucial role in progressing from coronary atherosclerosis to MI. The upregulation of TLR2 may have a favorable screening value for MI.
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Li et al. (2022) conducted a meta-analysis in Myocardial infarction (n=631). TLR2 expression vs. Non-MI controls was evaluated on Comprehensive expression level of TLR2 (SMD 2.55, 95% CI 1.35-3.75). TLR2 expression was significantly upregulated in patients with myocardial infarction compared to healthy controls, with a standardized mean difference of 2.55 and an AUC of 0.76.
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