Pathway link FOXO-LONGEVITY

FOXO1/3 → Longevity

FOXO1/3 activates Longevity.

Part of how this pathway affects lifespan runs through stress-resistance genes switched on by FOXO – so far shown mainly in simple animals like worms, not yet in mammals.

Genetic TORC1 inhibition in C. elegans extends lifespan through BOTH SKN-1/Nrf and DAF-16/FoxO, which activate protective genes and raise stress resistance. Rapamycin does NOT work the same way: it triggers a similar protective response but extends worm lifespan dependent on SKN-1 and NOT on DAF-16, apparently by interfering with TORC2 alongside TORC1 (ROB2012). This FoxO arrow therefore holds for the genetic arm, not for the drug.

The conditions it holds under

An invertebrate result, and the two arms must not be merged. ROB2012's title reads 'TOR signaling and rapamycin influence longevity by regulating SKN-1/Nrf and DAF-16/FoxO', but its own abstract splits them: the DAF-16/FoxO requirement belongs to genetic TORC1 inhibition, while the rapamycin effect is SKN-1-dependent and DAF-16-INDEPENDENT. Not shown in mammals in this corpus.

Time it takes

long exposure (days to weeks)

Step

indirect (through steps not drawn here)

Measured in

C. elegans

Reaches people?

not tested in people

How settled

emerging, few independent studies

Studies behind it

Points the other way

No study in the Atlas contradicts this link. That means none in this curated set, not none in the literature.

Who has checked this

Checked by

No researcher outside the project has checked this link yet.

Curator sign-off

Not signed off yet. This link was drafted with AI help and has not been reviewed link by link; treat it as a proposal until it is.

Curated by

Oliver Barton, with AI help for drafting; see how links are checked.

“How settled” describes how far researchers in the field agree. It is not the same as the sign-off above, which only says whether a named curator has checked this page.

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