Cardiac Myocyte–Specific Expression of Inducible Nitric Oxide Synthase Protects Against Ischemia/Reperfusion Injury by Preventing Mitochondrial Permeability Transition | Zendy

Matthew West | Zendy; Gregg Rokosh | Zendy; Detlef Obal | Zendy; V. Murugesan | Zendy; Yu-Ting Xuan | Zendy; Bradford G. Hill | Zendy; Rachel J. Keith | Zendy; Jürgen Schrader | Zendy; Yiru Guo | Zendy; Daniel J. Conklin | Zendy; Sumanth D. Prabhu | Zendy; Jay L. Zweíer | Zendy; Roberto Bolli | Zendy; Aruni Bhatnagar | Zendy

Open Access

Cardiac Myocyte–Specific Expression of Inducible Nitric Oxide Synthase Protects Against Ischemia/Reperfusion Injury by Preventing Mitochondrial Permeability Transition

Author(s) -

Matthew West,

Gregg Rokosh,

Detlef Obal,

V. Murugesan,

Yu-Ting Xuan,

Bradford G. Hill,

Rachel J. Keith,

Jürgen Schrader,

Yiru Guo,

Daniel J. Conklin,

Sumanth D. Prabhu,

Jay L. Zweíer,

Roberto Bolli,

Aruni Bhatnagar

Publication year - 2008

Publication title -

circulation

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 7.795

H-Index - 607

eISSN - 1524-4539

pISSN - 0009-7322

DOI - 10.1161/circulationaha.108.791533

Subject(s) - mitochondrial permeability transition pore , cardioprotection , nitric oxide synthase , ischemia , reperfusion injury , medicine , mitochondrion , nitric oxide , pharmacology , genetically modified mouse , nad+ kinase , transgene , endocrinology , biology , biochemistry , apoptosis , programmed cell death , enzyme , gene

Inducible nitric oxide synthase (iNOS) is an obligatory mediator of the late phase of ischemic preconditioning, but the mechanisms of its cardioprotective actions are unknown. In addition, it remains unclear whether sustained elevation of iNOS in myocytes provides chronic protection against ischemia/reperfusion injury.

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