Abstract：
:Increased aerobic glycolysis in endothelial cells of atheroprone areas of blood vessels has been hypothesized to drive increased inflammation and lesion burden but direct links remain to be established. Here we show that endothelial cells exposed to disturbed flow in vivo and in vitro exhibit increased levels of protein kinase AMP-activated (PRKA)/AMP-activated protein kinases (AMPKs). Selective deletion of endothelial Prkaa1, coding for protein kinase AMP-activated catalytic subunit alpha1, reduces glycolysis, compromises endothelial cell proliferation, and accelerates the formation of atherosclerotic lesions in hyperlipidemic mice. Rescue of the impaired glycolysis in Prkaa1-deficient endothelial cells through Slc2a1 overexpression enhances endothelial cell viability and integrity of the endothelial cell barrier, and reverses susceptibility to atherosclerosis. In human endothelial cells, PRKAA1 is upregulated by disturbed flow, and silencing PRKAA1 reduces glycolysis and endothelial viability. Collectively, these results suggest that increased glycolysis in the endothelium of atheroprone arteries is a protective mechanism.
journal_name
Nat Communjournal_title
Nature communicationsauthors
Yang Q,Xu J,Ma Q,Liu Z,Sudhahar V,Cao Y,Wang L,Zeng X,Zhou Y,Zhang M,Xu Y,Wang Y,Weintraub NL,Zhang C,Fukai T,Wu C,Huang L,Han Z,Wang T,Fulton DJ,Hong M,Huo Ydoi
10.1038/s41467-018-07132-xsubject
Has Abstractpub_date
2018-11-07 00:00:00pages
4667issue
1issn
2041-1723pii
10.1038/s41467-018-07132-xjournal_volume
9pub_type
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