Will peroxisomal protein import (PRX-5) become a validated aging target with lifespan extension in mammals, and when?
Chance it happens
67%Belief the predicted event happens at all — every “yes / by-a-date” outcome added together. “Other” is tracked as its own third slice.
Outcomes
Resolution criteria
A peer-reviewed paper shows lifespan extension in mammals via restored peroxisomal protein import (PRX-5 or an ortholog). Resolution horizon: 2034-12-31. Source: peer-reviewed publication.
Description
PRX-5 is peroxin-5, the shuttle receptor that imports enzymes into the peroxisome — the tiny organelle that burns fatty acids and mops up reactive oxygen species. The enzymes are built out in the cytoplasm carrying a short address tag; PRX-5 reads that tag and hauls them inside. Lose the receptor and the peroxisome is a hollow shell: the enzymes exist but never reach the compartment where they do their work. The aging angle comes from a 2026 C. elegans study: PRX-5 import falls with age, and that drop alone reproduces an old animal's metabolism — swollen lipid droplets, failing mitochondria, and loss of the normal fasting response. Overexpressing PRX-5 preserved lipid handling and mitochondrial integrity, and the authors argue peroxisomal import causally underpins dietary-restriction lifespan extension. Nature Aging, 2026: https://www.nature.com/articles/s43587-026-01122-1 — earlier preprint: https://www.biorxiv.org/content/10.1101/2025.02.14.638340 That's worms, though. PRX-5's mammalian counterpart is PEX5, and its levels are known to fall in aged mouse brain neurons (https://pmc.ncbi.nlm.nih.gov/articles/PMC7484460/) — but no one has yet shown that restoring peroxisomal import extends a mammal's lifespan. That last step is exactly what this market asks. Resolution horizon: 2034.
Evidence & context
Trials, publications and reports our research found on this prognosis. Each links to the original source.
This appears to be a genuine peer-reviewed Nature Aging research article published on 2026-05-20. It is directly relevant because it links age-related loss of peroxisomal protein import (PRX-5/PEX5 pathway) to longevity biology and reports lifespan effects in C. elegans, but it does not satisfy the forecast resolution criterion because it does not show mammalian lifespan extension from restoring peroxisomal import.
This is a peer-reviewed 2017 publication on PEX5/peroxisomal protein import biology, describing how PEX5 responds to oxidative stress by altering catalase localization. It is relevant as mechanistic background for PRX-5/PEX5 as an aging-related target, but it does not itself report lifespan extension in mammals or target validation under the resolution criteria.
This is a bioRxiv preprint on the molecular mechanism of peroxisomal protein import via the PEX14/PEX5 interface, directly related to the target pathway in the prediction. It does not report mammalian lifespan extension or target validation, but it is still relevant background evidence on pathway tractability and mechanism.
This appears to be a peer-reviewed PMC-hosted research article on age-related reduction of PEX5, the peroxisomal protein import receptor, in mammalian cortical neurons. It bears on the forecast because it supports biological plausibility for PRX-5/PEX5 as an aging-related target, though it does not by itself demonstrate lifespan extension from restoring import.