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. 2025 Apr 6;56(6):1542–1553. doi: 10.1161/STROKEAHA.124.049808

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© 2025 The Authors.

Stroke is published on behalf of the American Heart Association, Inc., by Wolters Kluwer Health, Inc. This is an open access article under the terms of the Creative Commons Attribution License, which permits use, distribution, and reproduction in any medium, provided that the original work is properly cited.

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Figure 4. — A genetic proxy for high-molecular-weight kininogen (HMWK) recapitulates its role in factor XI stabilization, thrombin amplification, and increased risk of ischemic stroke, cardioembolic stroke (CES), and venous thromboembolism (VTE). A, Visualization of the structure of KNG1, the gene that encodes HMWK. Black bars represent exons, and gray bars represent introns. Genomic positions are provided according to the GRCh38 genome assembly. The red line marks the genomic position of the rs5030062 variant used to proxy HMWK levels. B, LocusZoom plots for regional associations of genetic variants with VTE, ischemic stroke, and plasma HMWK levels. Dots represent genetic variants, and the diamond represents the rs5030062 protein quantitative trait loci (pQTL). The x axis represents genomic position in the GRCh38 genome assembly, and the y axis represents the −log₁₀(P) for each variant association with the outcome. Genetic variants are colored according to their linkage disequilibrium estimate with the lead rs5030062 pQTL (using the 1000G European reference panel). C, Estimates for associations of the C allele of the rs5030062 variant with HMWK, prekallikrein, factor XI, and thrombin levels. D, Visualization of the effects of a genetically proxied 1-SD increase in HMWK levels on the relative risk of VTE, ischemic stroke, and cardioembolic stroke. This figure was created using the BioRender software (BioRender.com).