Proteome-Wide Genetic Investigation of Large Artery Stiffness

Marie Joe Dib, Joe David Azzo, Lei Zhao, Oday Salman, Sushrima Gan, Marc L. De Buyzere, Tim De Meyer, Christina Ebert, Kushan Gunawardhana, Laura Liu, David Gordon, Dietmar Seiffert, Chang Ching-Pin, Payman Zamani, Jordana B. Cohen, Bianca Pourmussa, Seavmeiyin Kun, Dipender Gill, Stephen Burgess, Vanessa van EmpelA. Mark Richards, Jaclyn Dennis, Ali Javaheri, Douglas L. Mann, Thomas P. Cappola, Ernst Rietzschel, Julio A. Chirinos

Research output: Contribution to journalArticlepeer-review

1 Scopus citations

Abstract

The molecular mechanisms contributing to large artery stiffness (LAS) are not fully understood. The aim of this study was to investigate the association between circulating plasma proteins and LAS using complementary proteomic and genomic analyses. A total of 106 proteins associated with carotid-femoral pulse-wave velocity, a noninvasive measure of LAS, were identified in 1,178 individuals from the Asklepios study cohort. Mendelian randomization analyses revealed causal effects of 13 genetically predicted plasma proteins on pulse pressure, including cartilage intermediate layer protein-2, high-temperature requirement A serine peptidase-1, and neuronal growth factor-1. These findings suggest potential novel therapeutic targets to reduce LAS and its related diseases.

Original languageEnglish
Pages (from-to)1178-1191
Number of pages14
JournalJACC: Basic to Translational Science
Volume9
Issue number10
DOIs
StatePublished - Oct 2024

Keywords

  • Asklepios study
  • Mendelian randomization
  • aortic stiffness
  • large artery stiffness
  • proteomics
  • pulse-wave velocity

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