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| Accelerated aging pathology in ad libitum fed Xpd^T^T^D mice is accompanied by features suggestive of caloric restriction [An article from: DNA Repair] | Digitalby S.W.P. Wijnhoven (Author), R.B. Beems (Author), M. Roodbergen (Author), van d (Author)
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Product Description
This digital document is a journal article from DNA Repair, published by Elsevier in . The article is delivered in HTML format and is available in your Amazon.com Media Library immediately after purchase. You can view it with any web browser.Description: Trichothiodystrophy (TTD) patients with a mutation in the XPD gene of nucleotide excision repair (NER) have a short life span and show various features of premature aging, thereby linking DNA damage to the aging process. Xpd^T^T^D mutant mice share many features with TTD patients, including a shorter life span, accompanied by a segmental progeroid phenotype. Here we report new pathology features supportive to the premature aging phenotype of Xpd^T^T^D mice. Strikingly, accelerated aging pathology is accompanied by signs suggestive of caloric restriction (CR), a condition usually linked to retardation of age-related pathology and life extension. Accelerated aging symptoms in Xpd^T^T^D mice are most likely due to accumulation of endogenously generated DNA damage and compromised transcription leading to cell death, whereas CR symptoms may reflect the need of Xpd^T^T^D mice to reduce metabolism (ROS production) in an attempt to extend their life span. Our current findings in Xpd^T^T^D mice further strengthen the link between DNA damage, repair and aging. |
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