Age-associated decline of Lamtor5 drives immunosenescence and systemic aging via cGAS-mediated paracrine inflammation.
What this study shows
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.
At a glance
| Evidence type | A Animal model Marked A because it is an animal intervention or observation study measuring an organismal outcome (model: Mouse); the code names the system studied -- animal work can be rigorous and still not be human data. |
| Study type | 4 - Animal Study |
| Model system | Mouse |
| Journal | Cell Death and Differentiation |
| Year | 2026 |
| Peer reviewed | Yes |
| Record last updated | 2026-07-29 |
| Source | DOI 10.1038/s41418-026-01823-5 · PMID 42463581 |
Extracted findings
These fields were extracted from the paper with AI assistance and have not been checked against the source. Read them as a pointer into the paper, not as curated claims; where they disagree with the curated summary above, the curated summary stands.
| Intervention | Lamtor5 overexpression / restoration |
| Target | Lamtor5 / mTORC1 Ragulator complex / cGAS-STING |
| Model | Mouse |
| Effect | Decline of Lamtor5 reduces mTOR activity in aging macrophages, promoting immunosenescence; Lamtor5 restoration reverses aging phenotypes |
In the Atlas
Related topics
Links in the pathway map
- Supports Ragulator inhibits cGAS-STING pathway
- Supports cGAS-STING pathway activates Cellular senescence
Open questions that cite this study
- Cited as supporting evidence for the open question How much of rapamycin's healthspan benefit runs through fewer senescent cells?.
- Cited as supporting evidence for the open question Is there a low-dose mTOR schedule whose immune effects come out favourable, compartment by compartment?.
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