Researchers at the University of Exeter report that key aspects of human cell aging can be reversed by new compounds they developed that target mitochondria. They also identified two splicing factors that play a key role in when and how endothelial cells become senescent.
"As human bodies age, they accumulate old (senescent) cells that do not function as well as younger cells," said Professor Lorna Harries. "This is not just an effect of ageing—it's a reason why we age.
"We used to think age-related diseases like cancer, dementia, and diabetes each had a unique cause, but they actually track back to one or two common mechanisms,” Harris explained. "This research focuses on one of these mechanisms, and the findings with our compounds have potentially opened up the way for new therapeutic approaches in the future.
In this research, published last month in Aging, the researchers were able to very specifically target two splicing factors (SRSF2 or HNRNPD) that play a key role in determining how and why our cells change with advancing age. "Nearly half of the aged cells we tested showed signs of rejuvenating into young cell models," said Professor Harries.
The researchers tested three different compounds and found each produced a 40-50% drop in the number of senescent blood vessel cells. These compounds were designed to selectively deliver minute quantities of hydrogen sulfide to the mitochondria in cells and help the old or damaged cells to generate the energy needed for survival and to reduce senescence.
"Our compounds provide mitochondria in cells with an alternative fuel to help them function properly," added Professor Matt Whiteman, also from the University of Exeter.
Image: Cellular senescence in human cells. Image courtesy of Eva Latorre.