Caffeine has been shown to slow the aging of yeast cells, which are often used as a model organism. The same effect is also explained by the link between coffee consumption and longer life in humans. Identifying the mechanisms by which caffeine affects cellular aging will help in the development of drugs for healthy aging without the side effects that caffeine has. Research published in the journal Microbial Cell.
The research was conducted on the yeast Schizosaccharomyces pombe, which is used as a model organism for studying human diseases and disorders associated with DNA damage and cell cycle disorders. The researchers focused specifically on how caffeine affects internal processes in the cell related to division and repair of gene damage. The same team of researchers previously suggested that caffeine affects mTORC1, a receptor that helps cells determine whether conditions are favorable for division and growth.
However, a new study has shown that caffeine does not affect mTORC1 directly, but through the AMPK pathway, which provides cells with energy when it is low. The scientists identified two checkpoints in this signaling pathway that caffeine affects: one is related to the repair of DNA damage, while the other is related to the duplication of DNA before division. The effect of caffeine on the repair of DNA damage was contradictory: on the one hand, it prevented DNA repair, and on the other, it made the cell more sensitive to damage to the genome.
Further studies in cells more closely related to humans will help better understand caffeine's role in protecting cells from aging. However, even if caffeine proves ineffective in fighting aging, drugs that target the AMPK pathway, such as the diabetes drug metformin, may prove useful.
