UConn professor explains why targeting a different type of senescent cell might produce more compelling lifespan and healthspan results.
The University of Connecticut is home to the UConn Center on Aging, a research organisation that aims to approach aging in a proactive, personalized way – guided by sound scientific principles. One of the key research areas explored at the center is the role that cellular senescence plays in various tissue dysfunctions associated with aging, obesity and other pathological conditions.

Recent studies by UConn researchers made the case for focusing on a previously unexplored type of protein expressed by senescent cells, and subsequently found that targeting cells expressing that protein showed potential to improve physical function and overcome insulin resistance.

Longevity.Technology: Most research into cellular senescence in mouse models has been focused on a tumor-suppressor protein called p16. After deciding to study the lesser-known p21 protein instead, the UConn team found that removing cells expressing p21 from the tissues of older mice improved their physical function. To learn more about this work, we caught up with Dr Ming Xu, assistant professor at UConn Center on Aging.

Xu has been studying senescence for more than a decade, and, like everyone else, initially spent most of his time looking at p16. This was largely because of a key 2011 study, which showed that clearance of senescent cells expressing p16 in aged mice delayed age-related disease.

“That work led to a bunch of drug development and a number of senolytics have been developed as a result,” says Xu. “I think there are at least 10 clinical trials going on right now, and we are all anxiously waiting for the results. But the whole field is still in its infancy – and there are a lot of unknowns. And I think that basing everything on the p16 mouse model is not enough.”