We found a match
Your institution may have access to this item. Find your institution then sign in to continue.
- Title
Thioredoxin overexpression in both the cytosol and mitochondria accelerates age-related disease and shortens lifespan in male C57BL/6 mice.
- Authors
Cunningham, Geneva M.; Flores, Lisa C.; Roman, Madeline G.; Cheng, Christie; Dube, Sara; Allen, Colton; Valentine, Joseph M.; Hubbard, Gene B.; Bai, Yidong; Saunders, Thomas L.; Ikeno, Yuji
- Abstract
To investigate the role of increased levels of thioredoxin (Trx) in both the cytosol (Trx1) and mitochondria (Trx2) on aging, we have conducted a study to examine survival and age-related diseases using male mice overexpressing Trx1 and Trx2 (TXNTg × TXN2Tg). Our study demonstrated that the upregulation of Trx in both the cytosol and mitochondria in male TXNTg × TXN2Tg C57BL/6 mice resulted in a significantly shorter lifespan compared to wild-type (WT) mice. Cross-sectional pathology data showed a slightly higher incidence of neoplastic diseases in TXNTg × TXN2Tg mice than WT mice. The incidence of lymphoma, a major neoplastic disease in C57BL/6 mice, was slightly higher in TXNTg × TXN2Tg mice than in WT mice, and more importantly, the severity of lymphoma was significantly higher in TXNTg × TXN2Tg mice compared to WT mice. Furthermore, the total number of histopathological changes in the whole body (disease burden) was significantly higher in TXNTg × TXN2Tg mice compared to WT mice. Therefore, our study suggests that overexpression of Trx in both the cytosol and mitochondria resulted in deleterious effects on aging and accelerated the development of age-related diseases, especially cancer, in male C57BL/6 mice.
- Publication
GeroScience, 2018, Vol 40, Issue 5/6, p453
- ISSN
2509-2715
- Publication type
Article
- DOI
10.1007/s11357-018-0039-6