Open AccessEndothelium-restricted endothelin-1 overexpression in type 1 diabetes worsens atherosclerosis and immune cell infiltration via NOX1
Author(s) -
Sofiane Ouerd,
Noureddine IdrisKhodja,
Michelle Trindade,
Nathanne S. Ferreira,
Olga Berillo,
Suellen C Coelho,
Mário Fritsch Neves,
Karin JandeleitDahm,
Pierre Paradis,
Ernesto L. Schiffrin
Publication year - 2020
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/cvaa168
Subject(s) - nox4 , apolipoprotein e , endocrinology , nadph oxidase , medicine , knockout mouse , oxidative stress , nox1 , streptozotocin , endothelium , inflammation , diabetes mellitus , biology , receptor , disease
NADPH oxidase (NOX) 1 but not NOX4-dependent oxidative stress plays a role in diabetic vascular disease, including atherosclerosis. Endothelin (ET)-1 has been implicated in diabetes-induced vascular complications. We showed that crossing mice overexpressing human ET-1 selectively in endothelium (eET-1) with apolipoprotein E knockout (Apoe-/-) mice enhanced high-fat diet-induced atherosclerosis in part by increasing oxidative stress. We tested the hypothesis that ET-1 overexpression in the endothelium would worsen atherosclerosis in type 1 diabetes through a mechanism involving NOX1 but not NOX4.