Heme Oxygenase-1 | Zendy

Philip Wenzel | Zendy; Matthias Oelze | Zendy; Meike Coldewey | Zendy; Marcus Hortmann | Zendy; Andreas Seeling | Zendy; Ulrich Hink | Zendy; Hanke Mollnau | Zendy; Dirk Stalleicken | Zendy; Henry Weiner | Zendy; Jochen Lehmann | Zendy; Huige Li | Zendy; Ulrich Förstermann | Zendy; Thomas Münzel | Zendy; Andreas Daiber | Zendy

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Heme Oxygenase-1

Author(s) -

Philip Wenzel,

Matthias Oelze,

Meike Coldewey,

Marcus Hortmann,

Andreas Seeling,

Ulrich Hink,

Hanke Mollnau,

Dirk Stalleicken,

Henry Weiner,

Jochen Lehmann,

Huige Li,

Ulrich Förstermann,

Thomas Münzel,

Andreas Daiber

Publication year - 2007

Publication title -

arteriosclerosis thrombosis and vascular biology

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 3.007

H-Index - 270

eISSN - 1524-4636

pISSN - 1079-5642

DOI - 10.1161/atvbaha.107.143909

Subject(s) - hemin , heme oxygenase , heme , nitric oxide , chemistry , reactive oxygen species , aldehyde dehydrogenase , pharmacology , hemeprotein , soluble guanylyl cyclase , biochemistry , nitrite , enzyme , nitrate , guanylate cyclase , biology , organic chemistry

Nitrate tolerance is likely attributable to an increased production of reactive oxygen species (ROS) leading to an inhibition of the mitochondrial aldehyde dehydrogenase (ALDH-2), representing the nitroglycerin (GTN) and pentaerythrityl tetranitrate (PETN) bioactivating enzyme, and to impaired nitric oxide bioactivity and signaling. We tested whether differences in their capacity to induce heme oxygenase-1 (HO-1) might explain why PETN and not GTN therapy is devoid of nitrate and cross-tolerance.

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