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Rapamycin decreases DNA damage accumulation and enhances cell growth of WRN-deficient human fibroblasts.
- Source :
- Aging Cell; Jun2014, Vol. 13 Issue 3, p573-575, 3p
- Publication Year :
- 2014
-
Abstract
- Werner syndrome (WS), caused by mutations at the WRN helicase gene, is a progeroid syndrome characterized by multiple features consistent with accelerated aging. Aberrant double-strand DNA damage repair leads to genomic instability and reduced replicative lifespan of somatic cells. We observed increased autophagy in WRN knockdown cells; this was further increased by short-term rapamycin treatment. Long-term rapamycin treatment resulted in improved growth rate, reduced accumulation of DNA damage foci and improved nuclear morphology; autophagy markers were reduced to near-normal levels, possibly due to clearance of damaged proteins. These data suggest that protein aggregation plays a role in the development of WS phenotypes and that the mammalian target of rapamycin complex 1 pathway is a potential therapeutic target of WS. [ABSTRACT FROM AUTHOR]
Details
- Language :
- English
- ISSN :
- 14749718
- Volume :
- 13
- Issue :
- 3
- Database :
- Complementary Index
- Journal :
- Aging Cell
- Publication Type :
- Academic Journal
- Accession number :
- 96151516
- Full Text :
- https://doi.org/10.1111/acel.12190