The steady march of aging might not have to be so steady, according to a growing body of research. Now a team from the University at Buffalo has isolated a single gene that controls senescence, the process that stops cells from dividing and contributes to aging symptoms. Ramping it up, they found how easily the effect can spread among neighboring cells. That makes the gene a crucial target for future work into anti-aging and cancer therapies.

Living cells have a natural limit to the amount of times they can divide, before they stop and become what are known as senescent cells. The problem is, over time these senescent cells build up in the body, eventually contributing to the physical symptoms we associate with aging, such as increased risk of diabetes, heart disease, arthritis and cataracts. On the other hand though, completely halting senescence can lead to cancer, as the cells continue to divide unchecked.

Realizing this mechanism, scientists have been developing ways to clear out these senescent cells, including a new class of drugs known as senolytics. In tests, these drugs have been found to extend the lifespan of mice by up to an impressive 35 percent, and keep them in better health for longer.

For the new study, the Buffalo team set out to catalogue all of the genes involved in senescence, particularly lipid-related genes. Through several experiments, one gene in particular popped up as an outlier: CD36. This gene's activity seems to go into overdrive in senescent cells, so the researchers tested how it was related to the phenomenon.

By ramping up the activity of CD36 in young, healthy cells, the team was able to make them stop dividing far earlier than they normally would. Interestingly, even when only 10 to 15 percent of cells were overexpressing CD36, the effect soon spread to almost every other cell in the petri dish. Even more worryingly, even when those senescent cells were cleared out and brand new ones placed in the same growth medium, the effect still lingered, spreading to the new cells as well.

A fluorescence microscope image of a human lung fibroblast cell that's been engineered to overexpress the CD36 gene (red spots) Darleny Lizardo/Alan Siegel/University at Buffalo North Campus Confocal Imaging Facility

"What we found was very surprising," says Ekin Atilla-Gokcumen, co-author of the study. "Senescence is a very complex process, and we didn't expect that altering expression of one gene could spark it, or cause the same effect in surrounding cells."

Speeding up the aging process is the exact opposite of what people want out of this kind of research, but the team says that it's important to confirm what role the CD36 gene plays, so future work can target it to try to undo the damage. Of course, that would include making sure we don't swing too far in the other direction and give ourselves cancer.

"Our research identifies CD36 as a candidate for further study. Senescence is a fundamental aspect of being a cell, but there is still a lot that we don't know about it," says Omer Gokcumen, an author of the study. "Senescence seems to have implications for old age and cancer, so understanding it is very important."

The research was published in the journal Molecular Omics.

Source: University of Buffalo