The Shrew's Two-Year Lifespan Might Hold the Key to Human Longevity

Gene regulation and expression could hold the keys to slowing aging, according to new research from the University of Rochester. Researchers at the university discovered two critical gene expression regulation mechanisms that contribute heavily to longevity. Scientists built a genetic profile of long-lived and short-lived rodents by studying various rodent species. Shrews, for example, have a very short lifespan, around two years. Naked mole rats, on the other hand, live up to 41 years. The researchers hoped genetic profiles might help explain the massive difference in lifespan among rodent species. 

The study revealed that long-lived species have low expression of genes involved in metabolism and inflammation. Conversely, genes that code for DNA repair and cellular structures were highly expressed. Short-lived species exhibited the opposite profile, showing high expression in metabolic genes and low expression in regenerative genes. 

The genes that reduced lifespan most significantly were found to be controlled by circadian rhythms; their expression is limited to a specific period during the day or night. For humans, this means that reducing the harmful effects of these genes may start by getting a good night’s sleep and avoiding too much light after sundown. 

The genes demonstrated to increase lifespan are controlled by the pluripotency network. The pluripotency network allows the body to repair itself by reprogramming somatic cells to become pluripotent stem cells, or cells that can become any cell in the body. Pluripotency and its underlying mechanisms are considered one of the most promising avenues of research in longevity science. 

With this study, the scientists at the University of Rochester have opened up new avenues for longevity research by identifying two new promising study targets. Activating the pluripotency network at will could be a viable path to treatment for several age-related disorders. Similarly, the forced deactivation of genes that reduce lifespan is a likely therapeutic approach for longevity-focused clinicians.