Scientists extend lifespan in roundworms — are humans next?
The roundworm Caenorhabditis elegans, a millimetre-long nematode commonly used in lab testing, recently enjoyed a boost in its lifespan when South Korean researchers tinkered with a couple of proteins involved in monitoring the energy used by its cells. Humans also have these proteins, offering up possibilities for developing longevity-promoting drugs.
The proteins VRK-1 and AMPK work in tandem in roundworm cells, with the former telling the latter to get to work by sticking a phosphate molecule on it. In turn, AMPK’s role is to monitor energy levels in cells when cellular energy is running low. In essence, VRK-1 regulates AMPK and AMPK regulates the cellular energy status.
Using a range of different biological research tools, including introducing foreign genes into the worm, researchers led by Professor Seung-Jae V Lee from the Korea Advanced Institute of Science and Technology (KAIST) were able to dial up and down the activity of the gene that tells cells to produce the VRK-1 protein. Their results were published in the journal Science Advances.
The colleagues confirmed that the overexpression, or increased production, of the VRK-1 protein boosted the lifespan of the C. elegans, which normally lives just two to three weeks, and the inhibition of VRK-1 production reduced its lifespan. They found that the activity of the VRK-1-to-AMPK cellular-energy monitoring process is increased in low cellular energy status by reduced mitochondrial respiration — the set of metabolic chemical reactions that make use of the oxygen the worm breathes to convert macronutrients from food into the energy ‘currency’ that cells spend to do everything they need to do.
It is already known that mitochondria, the energy-producing engine rooms in cells, play a crucial role in ageing, and declines in the functioning of mitochondria are associated with age-related diseases. At the same time, the mild inhibition of mitochondrial respiration has been shown to promote longevity in a range of species, including flies and mammals.
When the research team performed similar tinkering with cultured human cells, they found they could also replicate this ramping up and down of the VRK-1-to-AMPK process that occurs in roundworms. According to Prof Lee, “This raises the intriguing possibility that VRK-1 also functions as a factor in governing human longevity, and so perhaps we can start developing longevity-promoting drugs that alter the activity of VRK-1.”
At the very least, the research points scientists in an interesting direction for investigating new therapeutic strategies to combat metabolic disorders by targeting the modulation of VRK-1. Metabolic disorders involve the disruption of chemical reactions in the body, including diseases of the mitochondria.
But before metabolic disorder therapeutics or longevity drugs can be contemplated by scientists, further research still needs to be carried out to better understand how VRK-1 works to activate AMPK, as well as figure out the precise mechanics of how AMPK controls cellular energy.
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