Identification of Cardiometabolic Protein Biomarkers for Acute Myocardial Infarction Using Olink Proteomics
Journal of Inflammation Research
Cite this paper
Plain citation
Xin Tan, Xiangyu Wang, Shuai Xu, Yiyao Zeng, Ge Zhang, Anchen Xu, Yufeng Jiang, Hezi Jiang, Yahui Song, Jili Fan, Yangjun Fu, Xiaohong Bo, Huimin Fan, Yafeng Zhou. Identification of Cardiometabolic Protein Biomarkers for Acute Myocardial Infarction Using Olink Proteomics. Journal of Inflammation Research. 2025. https://doi.org/10.2147/jir.s495784
Research context and source limits
Limited evidence note. Only the source material identified below has been reviewed; this is not a complete Paper GEO V2 assessment.
Protein-discovery design and supplementary sensitivity checks; diagnostic and causal claims remain unverified.
Protein discovery and follow-up
The study measures 92 plasma proteins in an exploratory Olink discovery set of 20 acute myocardial infarction cases and 10 controls. It selects PCOLCE, FCN2, REG1A, DEFA1 and CRTAC1 for ELISA and transcriptomic comparisons. These are protein measurements, and the observational comparisons do not establish diagnostic utility, a clinical decision threshold, or a treatment effect.
What the MR supplement actually reports
Supplementary Table S2 reports nominal inverse-variance-weighted associations for FCN2 and DEFA1. Their MR-Egger and weighted-median tests are not significant at 0.05. These method-dependent exploratory findings do not establish causality or treatment targets; exposure units, multiplicity and instrument mapping remain unverified.
Source: Table S2, FCN2 and DEFA1 IVW, MR-Egger and weighted-median rows
Validation boundaries remain explicit
ELISA counts differ between the Methods/Table 1 and Figure 5: 125 versus 120 infarction cases. Supplementary Table S1 identifies GSE57338, while the main text names GSE57388, leaving accession-to-result mapping unresolved. Differential-expression methods specify FDR adjustment, but its mapping to reported result thresholds needs clarification. The audit therefore withholds diagnostic accuracy and causal-validation claims.
Source: Methods ELISA and Statistical Analysis; Table 1; Figure 5; ELISA Results
Evidence limits
- ELISA cohort size and GEO accession/result mapping are unresolved.
- Nominal IVW associations are not robustly replicated across the named sensitivity methods.
- Multiplicity, exposure units and instrument mapping are insufficient for a causal claim.
Provenance
- Article source — Official publisher or PMC full text reviewed locally. Methods: General Information and biomarker screening; Results: Identification of Cardiometabolic-Related Biomarkers and ELISA Validation
- Official supplementary material — Publisher-hosted supplementary document. Table S2, FCN2 and DEFA1 IVW, MR-Egger and weighted-median rows
Source review: 2026-10-27.
Verify publication identity
These records identify the same original work; database inclusion is not evidence of scientific validity or clinical benefit.