https://www.medicalnewstoday.com/articles/327352.phpWe had previously shown that the absence or impairment of CSB is also responsible for dysfunction of mitochondria, the power plant of cells," she explains. "This new study reveals the very same alterations in replicative senescence, a process strictly linked to physiological aging."
For their research, the team artificially reduced the amount of CSB protein in skin cells grown in laboratory cell culture. As a result, the cells stopped replicating and became senescent.
However, in control cells that the researchers left to divide, they also noticed that the levels of CSB gradually began to drop off.
"Depletion of CSB was surprising since we did not expect this protein to have a regulatory function, and that this regulatory capacity is mediated by the levels of the protein itself," Ricchetti told Medical News Today.
"We did not expect that lower levels of the functional protein have such a dramatic effect on proliferation of normal cells," she continued.
Ricchetti's research points to an epigenetic process, meaning that the DNA in the affected cells is modified without introducing mutations. This allows for changes in the activity of genes, effectively switching them on or off.
https://www.nature.com/articles/s41467-019-13314-y