Key result
Genetically predicted Lp(a) and PCSK9 levels are linked to increased atherosclerosis risk.
Why the study?
Do genetically predicted levels of circulating proteins affect atherosclerosis risk?
Observational
Do genetically predicted levels of circulating proteins affect atherosclerosis risk?
Mendelian randomization analysis confirms the causal role of circulating proteins like lipoprotein (a) and PCSK9 in atherosclerosis, supporting them as drug targets.
Atherosclerosis is a leading cause of cardiovascular diseases, necessitating the identification of novel therapeutic targets. By utilizing Mendelian randomization, the aim is to identify potential drug targets for the treatment of atherosclerosis. Using results from genomewide association studies and protein quantitative trait loci data, we genetically identified causal effects of levels of several circulating proteins on atherosclerosis risk, validated using multiple statistical approaches, and identified promising drug targets. These findings demonstrated promising targets worthy of further clinical study, especially lipoprotein (a) and proprotein convertase subtilisin/kexin type 9.
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Du et al. (2026) conducted an observational in Atherosclerosis. Circulating proteins (especially lipoprotein (a) and PCSK9) was evaluated on Atherosclerosis risk. Genetically predicted levels of circulating proteins, especially lipoprotein (a) and PCSK9, were causally associated with atherosclerosis risk, identifying them as promising drug targets.
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