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Activation of PPARδ prevents endothelial dysfunction induced by overexpression of amyloid-β precursor protein
Author(s) -
Livius V. d’Uscio,
Pritam Das,
Anantha V. Santhanam,
Tongrong He,
Steven G. Younkin,
Zvonimir S. Katušić
Publication year - 2012
Publication title -
cardiovascular research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.774
H-Index - 219
eISSN - 1755-3245
pISSN - 0008-6363
DOI - 10.1093/cvr/cvs266
Subject(s) - superoxide , endothelial dysfunction , nadph oxidase , endocrinology , chemistry , amyloid precursor protein , medicine , superoxide dismutase , nitric oxide , endothelium , tetrahydrobiopterin , oxidative stress , nitric oxide synthase , biology , biochemistry , alzheimer's disease , disease , enzyme
Existing evidence suggests that amyloid-β precursor protein (APP) causes endothelial dysfunction and contributes to pathogenesis of atherosclerosis. In the present study, experiments were designed to: (1) determine the mechanisms underlying endothelial dysfunction and (2) define the effects of peroxisome proliferator-activated receptor delta (PPARδ) ligand on endothelial function in transgenic Tg2576 mice overexpressing mutated human APP.

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