Why the study?
Although AMI triggers cardiomyocyte senescence and alters methylation modifications, the association between cellular senescence and demethylation remained unclear.
Population
AMI and control samples from public databases
Comparison
AMI vs control samples
Design
Bioinformatics and machine learning analysis with RT-qPCR validation
Key result
Bioinformatics analysis and experimental validation identified BCL3, MMP9, NAMPT, and TLR4 as significantly upregulated key biomarkers associated with cellular senescence and demethylation in acute myocardial infarction.
Authors
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These senescence biomarkers merit prospective validation in AMI; leaves open their prognostic or therapeutic utility.
Observational (n=133)
No
p-value: p=<0.05
Su et al. (2025) conducted an observational in Acute myocardial infarction (n=133). Biomarker identification (BCL3, MMP9, NAMPT, TLR4) vs. Healthy controls was evaluated on Differential expression of BCL3, MMP9, NAMPT, and TLR4 (p=<0.05). Bioinformatics analysis and experimental validation identified BCL3, MMP9, NAMPT, and TLR4 as significantly upregulated key biomarkers associated with cellular senescence and demethylation in acute myocardial infarction.