The process of aging, and how to stop it, has long puzzled scientists. However, in a new study, published in the journal EMBO Reports, researchers from Osaka University and Nara Medical University in Japan have identified a key repair pathway that prevents cells from premature aging.
Each of our cells acts as a tiny molecular factory that carries out all of the essential processes our bodies need to survive. However, like factories, the machinery in our cells can wear out over time. To combat this, our cells are fitted with their own internal garbage disposal stations, called lysosomes. These lysosomes are full of digestive enzymes that break down these spent cellular components, as well as other cellular debris.
This process is called "microautophagy," which directly translates to "micro-self-eating." In other words, the cell is destroying its own worn-out components at an intracellular level. Autophagy can also occur at a whole cell level, where entire cells are destroyed.
However, if the lysosome itself becomes damaged or worn out, these enzymes may leak and digest healthy cellular machinery. This can result in inflammation and, ultimately, cell death, so the lysosomes need to be kept in good shape.
In their new study, the team found that lysosomes are able to repair themselves using this same process of microautophagy, with the help of several cellular signaling molecules.
If part of the lysosome's membrane is in need of repair, Gamma-aminobutyric acid receptor-associated proteins, or GABARAPs, are recruited to the site of the damage. These proteins in turn mediate the assembly of the cellular repair machinery, called ESCRT. This then causes the damaged area of the lysosomal membrane to fold in on itself, allowing the lysosome to break down its own damaged components.
Once the repair job is complete, a protein called Serine-threonine kinase 38, or STK38, comes in to help disassemble the repair machinery.
By removing these signaling molecules, cells begin to age much faster, shortening the lifespan of their host animal (which, in the case of this study, was a microscopic worm called C. elegans).
Both GABARAP and STK38 are very similar among a range of different animals, indicating that their structure and function have been conserved by evolution. In other words, their role in maintaining lysosome integrity and preventing cellular aging is so important that any mutations in their structure would be disadvantageous for an organism's survival.
These findings shine a light on a previously unknown biochemical repair pathway and will be instrumental in informing new, effective treatments for age-related diseases and supporting healthy aging.
Uncommon Knowledge
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Pandora Dewan is a Senior Science Reporter at Newsweek based in London, UK. Her focus is reporting on science, health ... Read more
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