Endothelium-restricted endothelin-1 overexpression in type 1 diabetes worsens atherosclerosis and immune cell infiltration via NOX1 | Zendy

Sofiane Ouerd | Zendy; Noureddine Idris-Khodja | Zendy; Michelle Trindade | Zendy; Nathanne S. Ferreira | Zendy; Olga Berillo | Zendy; Suellen C Coelho | Zendy; Mário Fritsch Neves | Zendy; Karin JandeleitDahm | Zendy; Pierre Paradis | Zendy; Ernesto L. Schiffrin | Zendy

Open Access

Endothelium-restricted endothelin-1 overexpression in type 1 diabetes worsens atherosclerosis and immune cell infiltration via NOX1

Author(s) -

Sofiane Ouerd,

Noureddine Idris-Khodja,

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 , medicine , nadph oxidase , 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.

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