Fig. 3: Two-sample Mendelian randomisation analysis in the UK Biobank. | Nature Communications

Fig. 3: Two-sample Mendelian randomisation analysis in the UK Biobank.

From: Identification of plasma proteomic markers underlying polygenic risk of type 2 diabetes and related comorbidities

Fig. 3: Two-sample Mendelian randomisation analysis in the UK Biobank.The alternative text for this image may have been generated using AI.

A Type 2 diabetes (T2D) Mendelian randomisation (MR) with cis instruments for each protein as the exposure. B T2D MR with both cis and trans instruments for each protein as the exposure. C Cis colocalization using T2D and protein quantitative loci (pQTL) genome-wide association study (GWAS) information. D Coronary artery disease (CAD) MR with cis instruments for each protein as the exposure. E CAD MR with both cis and trans instruments for each protein as the exposure. F CAD colocalization using CAD and pQTL GWAS information. In the MR plots, four conventional MR methods are displayed (simple median, weighted median, IVW, MR-Egger), plus an additional MR method called MR-Link-2. All proteins displayed in this figure had a median p-value across the four conventional MR methods < 0.05 (FDR-adjusted) and no pleiotropy as detected by MR-Egger (MR-Egger intercept p-value > 0.05). For panels (A, B, D, and E), the points represent the causal estimate obtained by each MR method (in the log-odds scale) and error bars represent the 95% confidence interval calculated using the standard error for each MR estimate. Note that MR-Link-2 estimates are on a different scale than the other MR methods but show consistency in the direction of effect. Finally, “*” signifies proteins with colocalization evidence. For panels A through F, the exposure (protein) GWAS had a sample size of 34,557 European-ancestry UK Biobank participants, and the outcome GWAS (T2D, CAD) had a sample size of 409,048 non-overlapping European-ancestry UK Biobank participants.

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