Source: University of Exeter
Summary: A new research shows that some of the key aspects of aging of human cells can be reversed by new compounds. The findings raise the possibility of future treatments.
As human bodies age, they accumulate old (senescent) cells that do not function as well as younger cells. This is not just an effect of aging, it’s a reason why we age. It is thought that age-related diseases like cancer, dementia and diabetes each had a unique cause, but they actually track back to one or two common mechanisms. A new research shows that some of the key aspects of aging of human cells can be reversed by new compounds developed at the University of Exeter. In a laboratory study of endothelial cells, which line the inside of blood vessels – researchers tested compounds designed to target mitochondria (the “power stations” of cells). The findings raise the possibility of future treatments not only for blood vessels, which become stiffer as they age, raising the risk of problems including heart attacks and strokes, but also for other cells. The study findings were published in the journal Aging.
In the samples used in the study, the number of senescent cells (older cells that have deteriorated and stopped dividing) was reduced by up to 50%. The Exeter team also identified two splicing factors (a component of cells) that play a key role in when and how endothelial cells become senescent. The new research looked at precisely targeting and rejuvenating mitochondria in old cells. Each one of our genes is capable of making more than one product, and splicing factors are the genes that make the decision about which of these products are made. In this new work, using novel chemicals, 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. The research was funded by Dunhill Medical Trust and the Medical Research Council.
Prof. Matt Whiteman said, “Our compounds provide mitochondria in cells with an alternative fuel to help them function properly; many disease states can essentially be viewed as accelerated aging, and keeping mitochondria healthy helps either prevent or, in many cases using animal models, reverse this.”
More Information: Eva Latorre et al, “Mitochondria-targeted hydrogen sulfide attenuates endothelial senescence by selective induction of splicing factors HNRNPD and SRSF2”, Aging (2018). DOI: 10.18632/aging.101500