Fig. 1 | Nature Communications

Fig. 1

From: Genome‐wide mapping of plasma protein QTLs identifies putatively causal genes and pathways for cardiovascular disease

Fig. 1

Flowchart of Study Design. (1) Selection and measurement of 71 high-value plasma proteins for atherosclerotic CVD via multiplex immunoassays in 7333 FHS participants, (2) GWAS of the 71 proteins in 6861 FHS participants to identify genome-wide significant pQTL variants, (3) independent external replication of sentinel pQTLs in INTERVAL, KORA, and previous GWAS, (4) colocalization and functional enrichment analyses of the identified pQTL variants, (5) integrated analysis of pQTL variants that coincide with CHD SNPs from GWAS, (6) identification of causal proteins for CHD using Mendelian randomization, (7) association analyses of proteins from steps 5 and 6 with risk for new-onset CHD/CVD events in 3520 FHS participants 50 years of age or older with available long-term follow-up. CHD coronary heart disease, CVD cardiovascular disease, FHS Framingham Heart Study, GWAS genome-wide association study, pQTL protein quantitative trait locus, SNP single-nucleotide polymorphism

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