An ANGPTL8-AKT2-mTOR Axis Drives Adipose Senescence and Aging-Related Functional Decline
What this study shows
Identifies ANGPTL8 as an endocrine driver of adipose-tissue aging: circulating ANGPTL8 tracked with biological age and mortality risk in a large human cohort, and genetic deletion of Angptl8 in mice extended lifespan and reduced senescence markers. Mechanistically, ANGPTL8 binds AKT2 and drives the AKT-mTOR-S6K axis to promote adipocyte senescence; blocking that axis abolished the pro-senescent effect.
At a glance
| Evidence type | A Animal model Marked A because it is an animal intervention or observation study measuring an organismal outcome (model: Human cohort (correlation) + mouse (Angptl8-/- knockout, lifespan) + primary adipocyte/cell studies); the code names the system studied -- animal work can be rigorous and still not be human data. |
| Study type | 4 - Animal Study |
| Model system | Human cohort (correlation) + mouse (Angptl8-/- knockout, lifespan) + primary adipocyte/cell studies |
| Journal | Aging Cell |
| Year | 2026 |
| Peer reviewed | Yes |
| Record last updated | 2026-08-22 |
| Source | DOI 10.1111/acel.70671 · PMID 42605193 |