Researchers have found an antiaging function in a protein deep within human cells.
Researchers at The University of Queensland in Australia have have discovered that a protein can controls the fine balance between the creation of new mitochondria and the repair of damaged mitochondria.
Longevity.Technology: Mitochondria, the powerhouses of our cells, crank out the energy we use to move, grow and repair. However, as we get older, age-related changes in our mitochondria occur which are associated with a decline in mitochondrial function. This impaired function is characterized by lowered oxidative capacity, decreased cellular energy production, significant increase in reactive oxygen species generation and diminished antioxidant defense [1].
The blame for increasing mitochondrial dysfunction can be partly laid at the feet of mitochondrial DNA. Mitochondria have their own DNA, but as we age, its volume, integrity and functionality decrease as it accumulates mutations and incurs damage. And the mitochondrial story is further complicated by the fact that the toxic by-products produced by the energy production process contribute to the rate at which the cell ages.
Associate Professor Steven Zuryn and Dr Michael Dai at the Queensland Brain Institute have discovered that a protein called ATSF-1 plays an important role when it comes to mitigating mitochondrial dysfunction [2].
“In conditions of stress, when mitochondrial DNA has been damaged, the ATSF-1 protein prioritises repair which promotes cellular health and longevity,” Dr Zuryn said, likening the relationship to a race car needing a pitstop.
“ATSF-1 makes the call that a pitstop is needed for the cell when mitochondria need repairs,” he said [3].
“We studied ATFS-1 in C. elegans, or round worms and saw that enhancing its function promoted cellular health, meaning the worms became more agile for longer. They didn’t live longer, but they were healthier as they aged.
“Mitochondrial dysfunction lies at the core of many human diseases, including common age-related diseases such as dementias and Parkinson’s,” said Dr Zuryn adding that the findings, which have been published in Nature Cell Biology, could have exciting implications for healthy aging and for possible therapies for people with inherited mitochondrial diseases.
Understanding how cells promote repair is an important step towards identifying possible interventions to prevent mitochondrial damage.
“Our goal is to prolong the tissue and organ functions that typically decline during ageing by understanding how deteriorating mitochondria contribute to this process,” Dr Dai said.
“We may ultimately design interventions that keep mitochondrial DNA healthier for longer, improving our quality of life.
[1] https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4003832/
[2] https://www.nature.com/articles/s41556-023-01192-y
[3] bit.ly/3Q3zxCe
