Free radicals are often blamed for causing cellular damage that promotes aging. A new study published today in Cell Metabolism suggests that they don't wreak cellular havoc, but plug into specific signaling pathways involved in aging.

Gaelle Laurent at the Curie Institute in Paris and colleagues created knockout mice missing gene that protects cells against oxidative stress, JunD. The mice aged prematurely and also had higher insulin levels than normal. Free radicals also accumulated in the insulin producing beta-cells in the knockouts' pancreas, which in turn promoted the growth of new blood vessels there. The researchers found that antioxidants decreased the levels of free radicals, but also of insulin. In other words, free radicals may act as a signal that promotes angiogenesis; the researchers think the signals turned by free radicals feed back into the pancreas and increase insulin levels.

Insulin is linked to aging via the FoxO gene, thought to be protective against aging. So the researchers also looked at FoxO levels in the livers of the JunD knockouts, observing that the gene showed lower expression in the liver. That could account for many of the signs of aging these mice showed, such as cataracts, hair graying and hair loss, lymphomas and premature death.

The study is interesting because it's a rare example of an aging effect caused by free radicals participating in cellular signaling, rather than by damaging cellular components, said Toren Finkel, who studies the molecular basis of aging at the National Heart and Lung Institute and was not involved in the research.

The fact that insulin and free radical pathways may be connected "is reassuring," said Finkel. It means that there could be "some common mechanisms that can be targeted," by pharmacological approaches to mediate the aging processes.