The lifespans of Caenorhabditis elegans (C. elegans) has been successfully manipulated by altering the VRK-1 protein, thus providing a potential target for anti-ageing drugs.
Alteration of the activity of proteins found in C. elegans a nematode a type of roundworm, commonly used in laboratory testing. Scientists have successfully clamped down the lifespans. The regulation was based on specific instructions to convert sugar into energy on a basis of cellular energy deficiency. This is a major milestone because humans possess similar proteins which can be targeted by anti-ageing drugs.
The proteins VRK-1 and AMPK work in unison in roundworm cells. The task of VRK-1 is to inform AMPK to initiate its processes by sticking a phosphate molecule, composed of one phosphorus and four oxygen atoms, on it. In turn, AMPK’s role is to oversee energy levels in cells, when cellular energy is running low. In essence, VRK-1 regulates AMPK, and AMPK regulates the cellular energy status.
Following a series of different biological research tools, not limited to introducing foreing genes into the worm, the scientists successfully raised the activity of the gene that instructs the cells to manufacture the VRK-1 protein.
In this way it was possible to confirm overexpression, or increased production of the protein VRK-1, boosted the lifespan of the nematode to higher than three weeks, also it was observed that the inhibition on VRK-1 production reduced the worms lifespan.
The study elicited that the activity of VRK-1-to-AMPK cellular-energy monitoringprocess increases in low cellular energy status by reducing mitochondrial respiration. The set of metabolic chemical reactions that make use of the oxygen the worm breathes to convert macronutrients from food into energy.
It is been established previously that the mitochondria plays an essential role in ageing and declines in its functioning is associated with age-related diseases. The mild inhibition of mitochondrial respiration has been shown to promote longevity in a range of species, including flies and mammals.
A similar experiment was conducted using cultures human cells, the findings were that it was possible to replicate this ramping up and down of the VRK-1-to-AMPK process that occurs in roundworms. This is interesting because it opens the door to the possibility that VRK-1 also functions as a factor in governing human longevity and so perhaps it would be possible to develop longevity-promoting drugs that alter the activity of VRK-1.
This study leads to new therapeutic possibilities for 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.