The histone demethylase Jarid1b mediates angiotensin II-induced endothelial dysfunction by controlling the 3'UTR of soluble epoxide hydrolase.

Andrea E VasconezPatrick JanetzkoJames A OoBeatrice Pflüger-MüllerCorina RatiuLunda GuKristian HelinGerd GeisslingerIngrid FlemingKatrin SchröderChristian ForkRalf P BrandesMatthias S Leisegang

Published in: Acta physiologica (Oxford, England) (2018)

Jarid1b contributes to the pro-inflammatory effects of AngII by stabilizing sEH expression. Jarid1b inhibition might be an option for future therapeutics against cardiovascular dysfunction.

Keyphrases

angiotensin ii
angiotensin converting enzyme
vascular smooth muscle cells
poor prognosis
diabetic rats
high glucose
dna methylation
oxidative stress
small molecule
current status
binding protein
gene expression
endothelial cells
stress induced