An international team of scientists led by Joao Passos at Newcastle University has for the first time shown that mitochondria (the “batteries” of the cells) are major triggers for aging, and eliminating them upon the induction of senescence prevents senescence in the aging mouse liver. This could lead to new therapies to combat age related disease.
As we grow old, cells in our bodies accumulate different types of damage and have increased inflammation, factors that are thought to contribute to the aging process.
As described Feb. 4 in an open-access paper in the EMBO Journal, the team carried out a series of genetic experiments involving human cells grown in the laboratory and succeeded in eliminating the majority, if not all, the mitochondria from aging cells.
Cells can normally eliminate faulty mitochondria by a process called mitophagy. The scientists were able to “trick” the cells into inducing this process in a grand scale, until all the mitochondria within the cells were physically removed.
To their surprise, they observed that the aging cells, after losing their mitochondria, showed characteristics similar to younger cells, that is, they became rejuvenated. The levels of inflammatory molecules, oxygen free radicals and expression of genes, which are among the makers of cellular aging, dropped to the level that would be expected in younger cells.
“This is a very exciting and surprising discovery,” said Passos. “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.”
The team, involving other universities in the UK and the U.S., also deciphered a new mechanism by which mitochondria contribute to aging: mitochondrial biogenesis, the complex process by which mitochondria replicate themselves, is a major driver of cellular aging.