Journal
AGING CELL
Volume 13, Issue 3, Pages 573-575Publisher
WILEY-BLACKWELL
DOI: 10.1111/acel.12190
Keywords
autophagy; DNA damage; mammalian target of rapamycin; rapamycin; Werner syndrome
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Funding
- NIH [R24CA78088/R24AG042328]
- Ellison Medical Foundation
- American Heart Association
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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.
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