Caspase-2 deficiency enhances aging-related traits in mice.
Authors: Zhang Y; Padalecki SS; Chaudhuri AR; De Waal E; Goins BA; Grubbs B; Ikeno Y; Richardson A; Mundy GR; Herman B Year: 2007 Journal: Mechanisms of ageing and development Abstract: 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. Reference
Integration:
Created on Jan. 3, 2013, 5:33 p.m. Not linked Integrated: False
Comment on This Data Unit