期刊
MECHANISMS OF AGEING AND DEVELOPMENT
卷 128, 期 2, 页码 213-221出版社
ELSEVIER IRELAND LTD
DOI: 10.1016/j.mad.2006.11.030
关键词
caspase-2; maximum lifespan; bone; hair growth; fat
资金
- NCI NIH HHS [P01 CA040035, P30 CA054174] Funding Source: Medline
- NIA NIH HHS [R37 AG007218, P01 AG019316, P01AG019316] Funding Source: Medline
Alteration of apoptotic activity has been observed in a number of tissues in aging mammals, but it remains unclear whether and/or how apoptosis may affect aging. Caspase-2 is a member of the cysteine protease family that plays a critical role in apoptosis. To understand the impact of compromised apoptosis function on mammalian aging, we conducted a comparative study on caspase-2 deficient mice and their wild-type littermates with a specific focus on the aging-related traits at advanced ages. We found that caspase-2 deficiency enhanced a number of traits commonly seen in premature aging animals. Loss of caspase-2 was associated with shortened maximum lifespan, impaired hair growth, increased bone loss, and reduced body fat content. In addition, we found that the livers of caspase-2 deficient mice had higher levels of oxidized proteins than those of age-matched wild-type mice, suggesting that caspase-2 deficiency compromised the animal's ability to clear oxidatively damaged cells. Collectively, these results suggest that caspase-2 deficiency affects aging in the mice. This study thus demonstrates for the first time that disruption of a key apoptotic gene has a significant impact on aging. (c) 2006 Elsevier Ireland Ltd. All rights reserved.
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