| First Author | Zhang Y | Year | 2007 |
| Journal | Mech Ageing Dev | Volume | 128 |
| Issue | 2 | Pages | 213-21 |
| PubMed ID | 17188333 | Mgi Jnum | J:119928 |
| Mgi Id | MGI:3703472 | Doi | 10.1016/j.mad.2006.11.030 |
| Citation | Zhang Y, et al. (2007) Caspase-2 deficiency enhances aging-related traits in mice. Mech Ageing Dev 128(2):213-21 |
| abstractText | 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. |
