Scientists discover anti-ageing protein that stops ‘zombie’ cells that can trigger cancer and Alzheimer’s disease
- Until now, experts believed that the protein TFEB helped regulate two important organelles
- Now researchers have identified the HKCD1 that helps zap persistent cells
Scientists have discovered a protein that can stop the formation of 'zombie cells' and slow down the aging process.
As we age, some cells live longer than they should and instead of being cleared away, they linger in the body, causing a buildup of cellular waste.
These so-called zombie cells increase the risk of age-related diseases, including Alzheimer's disease, heart failure and some cancers.
Now researchers in Japan have discovered that a protein called HKDC1 is essential for sucking up damaged mitochondria — the powerhouse of cells — and repairing lysosomes, which are needed to break down and clean up worn-out cell parts.
As we age, some cells live longer than necessary and remain in the body, rather than being cleared away, causing a buildup of cellular waste.
When mitochondria and lysosomes don't work as they should, cells don't function as they should and they become zombies.
A 'tidy cell appears to keep aging at bay', which means that drugs that target HKDC1 could treat age-related diseases, according to the scientists.
Until now, researchers did not fully understand how mitochondria and lysosomes were regulated.
However, they knew that a protein called transcription factor EB (TFEB) was involved.
Scientists from Osaka University discovered this HKDC1 is critical to helping increase levels of TFEB, keeping the levels of these two organelles in check and 'preventing cellular senescence' – when cells live longer than they should.
Writing in the journal Proceedings of the National Academy of Sciences, the researchers found that low levels of HKDC1 resulted in 'mitochondrial dysfunction' and 'the accumulation of damaged lysosome'.
At sufficient levels, by preventing cells from hanging around for too long, the protein “effectively helps remove mitochondrial waste” and “helps lysosomes recover from damage.”
Senior author Shuhei Nakamura, assistant professor in the department of genetics, said: 'Lysosomes and mitochondria contact each other through proteins called VDACs.
'In concrete terms, HKDC1 is responsible for the interaction with the VDACs. This protein is essential for the contact between the mitochondria and the lysosome, and therefore for lysosomal repair.'
The researchers now hope that the findings could pave the way for new treatments to combat aging-related conditions.
Drugs that increase levels of HKDC1 may therefore promote cell health and the aging process, the study suggests.