Mitochondrial Thioredoxin Reductase Is Essential for Early Postischemic Myocardial Protection | Zendy

Jan Horstkotte | Zendy; Tamara Perisic | Zendy; Manuela Schneider | Zendy; Philipp S. Lange | Zendy; Melanie Schroeder | Zendy; Claudia Kiermayer | Zendy; Rabea Hinkel | Zendy; Tilman Ziegler | Zendy; Pankaj Kumar Mandal | Zendy; Robert David | Zendy; Sabine Schulz | Zendy; Sabine Schmitt | Zendy; Julian D. Widder | Zendy; Fred Sinowatz | Zendy; Bernhard F. Becker | Zendy; Johann Bauersachs | Zendy; M Naebauer | Zendy; Wolfgang M. Franz | Zendy; Irmela Jeremias | Zendy; Markus Brielmeier | Zendy; Hans Zischka | Zendy; Marcus Conrad | Zendy; Christian Kupatt | Zendy

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Mitochondrial Thioredoxin Reductase Is Essential for Early Postischemic Myocardial Protection

Author(s) -

Jan Horstkotte,

Tamara Perisic,

Manuela Schneider,

Philipp S. Lange,

Melanie Schroeder,

Claudia Kiermayer,

Rabea Hinkel,

Tilman Ziegler,

Pankaj Kumar Mandal,

Robert David,

Sabine Schulz,

Sabine Schmitt,

Julian D. Widder,

Fred Sinowatz,

Bernhard F. Becker,

Johann Bauersachs,

M Naebauer,

Wolfgang M. Franz,

Irmela Jeremias,

Markus Brielmeier,

Hans Zischka,

Marcus Conrad,

Christian Kupatt

Publication year - 2011

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.111.059253

Subject(s) - mitochondrial permeability transition pore , reactive oxygen species , reperfusion injury , medicine , thioredoxin reductase , oxidative stress , thioredoxin , mitochondrial ros , ischemia , mitochondrion , pharmacology , microbiology and biotechnology , biology , programmed cell death , apoptosis , biochemistry

Excessive formation of reactive oxygen species contributes to tissue injury and functional deterioration after myocardial ischemia/reperfusion. Especially, mitochondrial reactive oxygen species are capable of opening the mitochondrial permeability transition pore, a harmful event in cardiac ischemia/reperfusion. Thioredoxins are key players in the cardiac defense against oxidative stress. Mutations in the mitochondrial thioredoxin reductase (thioredoxin reductase-2, Txnrd2) gene have been recently identified to cause dilated cardiomyopathy in patients. Here, we investigated whether mitochondrial thioredoxin reductase is protective against myocardial ischemia/reperfusion injury.

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