Inhibition of peroxisomal protein PRX-11 promotes longevity in Caenorhabditis elegans via enhancements to mitochondria (IMAGE)
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Figure 7. Model for the role of PRX-11 in regulating peroxisome degradation and mitochondrial homeostasis during aging. The schematic in the left panel illustrates that PRX-11 promotes age-associated peroxisome degradation and, in doing so, likely contributes to mitochondrial fragmentation and functional decline in older wild-type animals. Mitochondrial fragmentation and dysfunction can, in turn, drive further pexophagy. The schematic in the right panel illustrates that loss of PRX-11 activity, via gene knockdown or mutation, inhibits pexophagy and preserves peroxisome abundance in older animals, thereby supporting enhanced mitochondrial integrity and lifespan extension. The effects of peroxisome retention on mitochondria quality with age involve crosstalk between the two organelles, potentially mediated by changes to physical interactions or metabolic signaling.
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