The FES Gene at the 15q26 Coronary-Artery-Disease Locus Inhibits Atherosclerosis.
Elisavet KaramanaviDavid G McVeySander W van der LaanPaulina J StanczykGavin E MorrisYifan WangWei YangKenneth ChanRobin N PostonJun LuoXinmiao ZhouPeng GongPeter D JonesJunjun CaoRenata B KostogrysThomas R WebbGerard PasterkampHaojie YuQingzhong XiaoPeter A GreerEmma J StringerNilesh J SamaniShu YePublished in: Circulation research (2022)
We provide substantial evidence that the CAD risk variants at the 15q26.1 locus reduce FES expression in monocytes and that FES depletion results in larger atherosclerotic plaques with more monocytes/macrophages and smooth muscle cells. This study is the first demonstration that FES plays a protective role against atherosclerosis and suggests that enhancing FES activity could be a potentially novel therapeutic approach for CAD intervention.
Keyphrases
- coronary artery disease
- cardiovascular disease
- copy number
- randomized controlled trial
- poor prognosis
- dendritic cells
- percutaneous coronary intervention
- cardiovascular events
- coronary artery bypass grafting
- type diabetes
- genome wide
- immune response
- gene expression
- heart failure
- acute coronary syndrome
- dna methylation
- genome wide association study
- binding protein
- transcription factor
- aortic stenosis