, which is increasingly expressed during aging and in age-associated diseases. In this issue of the
, Norman Sharpless and colleagues at the University of North Carolina evaluated potential age-promoting compounds, including arsenic, a high-fat diet, UV light, and cigarette smoke in
The authors found that a high fat diet did not accelerate p16INK4
expression, but both UV light exposure and cigarette smoke exposure dramatically increased p16INK4
expression compared to controls that had not been exposed to these age-promoting compounds. This study demonstrates that p16LUC
mice are an appropriate model system for evaluating potential age-promoting compounds.