Pathway link CGASSTING-SENESCENCE
cGAS-STING pathway Cellular senescence
cGAS-STING pathway activates Cellular senescence.
In aged immune cells called macrophages, cGAS-STING switches on an inflammatory programme that spreads to neighbouring cells, so the ageing effect does not stay in the cell where it started. This comes from a single mouse study, and whether the same spread happens in human tissue has not been tested.
The conditions it holds under
Single mouse study; the human magnitude of this effect, and whether the same paracrine spread occurs in human tissue, are untested.
- Time it takes
- days
- Step
- indirect (through steps not drawn here)
- Measured in
- mouse
- Reaches people?
- not tested in people
- How settled
- emerging, few independent studies
Studies behind it
| Year | Evidence | Study |
|---|---|---|
| 2026 | A | Age-associated decline of Lamtor5 drives immunosenescence and systemic aging via cGAS-mediated paracrine inflammation.LV2026 Age-driven loss of Lamtor5, a key lysosomal mTOR activation complex subunit, drives macrophage immunosenescence and systemic aging phenotypes in mice by unleashing cGAS-STING paracrine inflammation; restoring Lamtor5 in aged mice rescued immunosenescence and attenuated systemic ageing phenotypes. |
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.
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