Researchers from the University of Rochester who are interested in longevity genetics propose new targets to fight aging and age-related disorders.
Mammals that age at vastly different rates have been created through natural selection. Naked mole rats, for instance, may live up to 41 years, which is over 10 times longer than mice and other rodents of comparable size.
What causes a longer lifespan? A crucial component of the puzzle, according to a recent study by biologists at the University of Rochester, is found in the mechanisms that control gene expression.
Vera Gorbunova, the Doris Johns Cherry professor of biology and medicine, Andrei Seluanov, the first author of the publication, Jinlong Lu, a postdoctoral research fellow in Gorbunova’s lab, and other researchers looked into genes related to longevity in a recent paper published in Cell Metabolism.
Their findings indicated that two regulatory mechanisms governing gene expression, known as the circadian and pluripotency networks, are crucial to longevity. The discoveries have significance for understanding how longevity arises as well as for providing new targets to fight aging and age-related disorders.
Comparing longevity genes
With maximum lifespans ranging from two years (shrews) to 41 years (naked mole rats), the researchers analyzed the gene expression patterns of 26 mammalian species. They discovered thousands of genes that either correlated positively or negatively with longevity and were linked to a species’ maximum lifetime.
They found that long-lived species tend to have low expression of genes involved in energy metabolism and inflammation; and high expression of genes involved in DOI: 10.1016/j.cmet.2022.04.011
The study was funded by the National Institute on Aging.