To prevent unwanted side effects, researchers try to figure out how rapamycin, which is normally used in cancer therapy and after organ transplants, extend lifespan. "We know that rapamycin extends lifespan via two mechanisms: increased autophagy and decreased activity of a protein called S6K. It has been shown that mice with altered S6K live longer." says Sebastian Grönke, co-author of the study.
An altered activity of S6K influences the endolysosomes that break down material in the cells and play an important role in regulating various cellular processes, such as inflammatory reactions. "When we suppressed S6K activity or the inflammatory signalling in the fat body, the flies lived longer, showed better immune function at old age and were able to clear bacterial infections more efficiently," explains Pingze Zhang, first author of the study. "Ultimately, we assume that the endolysosomes prevent the age-related increase in pro-inflammatory factors and that this is precisely where rapamycin attacks," concludes Sebastian Grönke.
The researchers also identified an important link between the endolysosomal system and age-related inflammation: the protein syntaxin 13. This protein is increased in the liver of rapamycin-treated mice, suggesting that the regulation of the endolysosomal system and the control of inflammatory pathways during ageing is similar between flies and mice.
From: EurekAlert!
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