![Cellular senescence serves as an important anticancer growth arrest mechanism, but also contributes to aging. This new study shows that mitochondria are necessary for the pro-inflammatory phenotype during senescence and that senescence can be induced by mitochondrial biogenesis. [EMBO J. February 2016 e201592862]](https://genengnews.com/wp-content/uploads/2018/08/graphic15916912916-1.gif)
Cellular senescence serves as an important anticancer growth arrest mechanism, but also contributes to aging. This new study shows that mitochondria are necessary for the pro-inflammatory phenotype during senescence and that senescence can be induced by mitochondrial biogenesis. [EMBO J. February 2016 e201592862]
George Burns was famously quoted that “you can’t help getting older, but you don’t have to get old.” A group of researchers led by scientists at the Newcastle University Institute for Ageing are hopeful that the comedian’s words will soon ring true.
This group of international investigators has recently described the cell’s battery, the mitochondria, as essential for the molecular aging process, often called senescence. The researchers found that when mitochondria were eliminated from aging cells, those cells reverted to a much younger phenotype—providing strong evidence that mitochondria are primary triggers of cell aging.
“This is a very exciting and surprising discovery,” remarked senior study author João Passos, Ph.D., a lecturer at the Newcastle University Institute for Ageing. “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.”
The findings from this study were published online today in EMBO through an article entitled “Mitochondria are required for pro-ageing features of the senescent phenotype.”
As cells within the body age, they accumulate various types of damage, which typically leads to increased inflammatory compounds thought to contribute to the aging process.
Dr. Passos and his colleagues conducted a series of genetic experiments involving human cells grown in vitro and successfully eliminated the majority, if not all, of the mitochondria from aging cells. Generally, cells can remove old or damaged mitochondria through a process called mitophagy, and the research team was able to take advantage of this pathway and induce it on a much larger scale—eliminating the organelle from the cell.
The researchers were surprised to observe 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.
“Here, we show the critical role of mitochondria in cellular senescence,” the authors wrote. “In multiple models of senescence, the absence of mitochondria reduced a spectrum of senescence effectors and phenotypes while preserving ATP production via enhanced glycolysis. Our results suggest that mitochondria are a candidate target for interventions to reduce the deleterious impact of senescence in aging tissues.”
The authors also identified that as cells grow old, mitochondrial biogenesis, the intricate process by which mitochondria replicate themselves, is a major driver of cellular aging.
Dr. Passos and his colleagues were excited by their findings and felt that this new study brings could be pivotal in designing compounds that target mitochondrial senescence.
“This is the first time that a study demonstrates that mitochondria are necessary for cellular aging,” explained lead author Clara Correia-Melo, Ph.D., postdoctoral research associate. “Now we are a step closer to devising therapies which target mitochondria to counteract the aging of cells.”
