Heart‐specific knockout of the mitochondrial thioredoxin reductase (Txnrd2) induces metabolic and contractile dysfunction in the aging myocardium
Ubiquitous deletion of thioredoxin reductase 2 (Txnrd2) in mice is embryonically lethal and associated with abnormal heart development, while constitutive, heart‐specific Txnrd2 inactivation leads to dilated cardiomyopathy and perinatal death. The significance of Txnrd2 in aging cardiomyocytes, howe...
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| Hauptverfasser: | , , , , , , , , , , , , |
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| Dokumenttyp: | Article (Journal) |
| Sprache: | Englisch |
| Veröffentlicht: |
21 Jul 2015
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| In: |
Journal of the American Heart Association
Year: 2015, Jahrgang: 4, Heft: 7 |
| ISSN: | 2047-9980 |
| DOI: | 10.1161/JAHA.115.002153 |
| Online-Zugang: | Resolving-System, lizenzpflichtig, Volltext: https://doi.org/10.1161/JAHA.115.002153 Verlag, lizenzpflichtig, Volltext: https://www.ahajournals.org/doi/10.1161/JAHA.115.002153 
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| Verfasserangaben: | Kiermayer Claudia, Northrup Emily, Schrewe Anja, Walch Axel, de Angelis Martin Hrabe, Schoensiegel Frank, Zischka Hans, Prehn Cornelia, Adamski Jerzy, Bekeredjian Raffi, Ivandic Boris, Kupatt Christian, Brielmeier Markus |
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| 520 | |a Ubiquitous deletion of thioredoxin reductase 2 (Txnrd2) in mice is embryonically lethal and associated with abnormal heart development, while constitutive, heart‐specific Txnrd2 inactivation leads to dilated cardiomyopathy and perinatal death. The significance of Txnrd2 in aging cardiomyocytes, however, has not yet been examined. | ||
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