The research could have broad implications in treating age-related illnesses, as well as cancer prevention.
For centuries people have sought ways to stave off the changes wrought by Father Time, particularly changes that lead to age-related diseases. This week, researchers at the University of Southern California believe they may have found a key to understand the aging process in the body, which could have significant implications in the prevention of age-related diseases, as well as cancers.
Coming out of the USC Viterbi School of Engineering, the researchers focused on senescence, a natural process in which cells permanently stop creating new cells. Senescence is one of the key causes of age-related decline, the researchers said. Senescence leads to the manifestations of various age-related diseases, including arthritis, osteoporosis and heart disease.
Nick Graham, assistant professor of Chemical Engineering and Materials Science, said in order for people to find the fountain of youth and drink from it, it’s important to know “where the fountain of youth is, and understand what the fountain of youth is doing.” But instead of looking for the fountain of youth, Graham said his team focused on understanding why cells age so they may be able to “design treatments for better aging.” The research from Graham’s team was recently published in the Journal of Biological Chemistry.
To understand how cells age, the researchers wanted to grasp the understanding of senescence. Lead author Alireza Delfarah, a graduate student in the Graham lab, described senescent cells as the opposite of stem cells. Stem cells, Delfarah said in a statement, have “unlimited potential for self-renewal or division.” Senescent cells, on the other hand, no longer divide and exist in an “irreversible state of cell cycle arrest.”
Graham’s team of researchers examined young cells that were thriving and fed them molecules labeled with stable isotopes of carbon. That was done in order to trace how the nutrients consumed by a cell were processed into different biochemical pathways, the researchers said.
According to the research, the team found that senescent cells stopped producing a class of chemicals called nucleotides, essential components of DNA. When the research team took younger cells and manipulated them to cease producing nucleotides, they became senescent. Delfarah said that revealed that nucleotides are essential to keep cells young. If in the future a way can be found to prevent cells from losing nucleotide synthesis, the cells might age more slowly, Delfarah noted.
Prior to this research, USC said senescence has primarily been studied in cells known as fibroblasts, which are the most common cells that make up the connective tissue in animals. Now Graham’s team wants to focus on how senescence occurs in epithelial cells, which is where cancers can often begin.
But the researchers do not want to stop senescence. That process plays an important role in arresting cancer. When cells become damaged and could morph into cancer, they can enter senescence in order to prevent the spread of cancer.
“Sometimes people talk about senescence as a double-edged sword, that it protects against cancer, and that’s a good thing,” Graham said in a statement. “But then it also promotes aging and diseases like diabetes, cardiac dysfunction or atherosclerosis and general tissue dysfunction. But then on the other hand, we would like to find a way to remove senescent cells to promote healthy aging and better function.”
