In a series of elaborate genetic experiments, Newcastle University scientists have shown, for the first time, that mitochondria are driving cellular aging. When the researchers removed mitochondria from aging cells, the cells took on a much younger appearance.
The study, published in the EMBO Journal and titled “Mitochondria are required for pro-ageing features of the senescent phenotype“, opens the path to developing therapies that counteract the cellular aging processes in disease by targeting mitochondria.
The aging process is characterized by the accumulation of damage to all the body’s cells. Damage that cannot be repaired remains in a cell, which increases cellular inflammation and, hence, the aging process.
Researchers, led by Dr. João Passos, used cultured human cells in which they managed to induce a process called mitophagy — normally responsible for eliminating damaged or faulty mitochondria. By triggering this process on a large-scale, the team managed to remove most, if not all, of the aging cells’ mitochondria.
They then noticed that the cells became revitalized, having characteristics of much younger cells. Comparing the mitochondria-free old cells to young cells, the team also observed that the levels of expression of genes known to drive aging, as well as the concentrations of inflammatory molecules and oxygen free radicals, were comparable in the two cell types.
“This is a very exciting and surprising discovery. We already had some clues that mitochondria played a role in the aging of cells, but scientists around the world have struggled to understand exactly how and to what extent these were involved. These new findings highlight that mitochondria are actually essential to the aging of cells,” said Dr. Passos in a press release.
Working with a number of U.S. and U.K. universities, the Newcastle team was also able to show that as cells grow older, the process of mitochondrial self-replication is driving cellular aging.
“This is the first time that a study demonstrates that mitochondria are necessary for cellular aging,” concluded Dr. Clara Correia-Melo, lead author of the study. “Now we are a step closer to devising therapies which target mitochondria to counteract the aging of cells.”