Atg5
Core gene required for autophagosome formation; overexpressing it in mice is sufficient to extend lifespan on its own.
A core gene needed to build the membrane sacs (autophagosomes) that carry out cellular cleanup. Simply making mice produce more of it - without any drug - was enough to extend their lifespan.
Core gene required for autophagosome formation; overexpressing it in mice is sufficient to extend lifespan on its own.
TL;DR. Atg5 appears in 3 curated studies in Oliver's mTOR Atlas: 2 in animal models; 1 preprint, not peer-reviewed. No study in people is recorded for it in the Atlas yet.
Evidence at a glance
| Evidence | What it means | Studies |
|---|---|---|
| A | Animal model | 2 |
| PP | Preprint, not peer-reviewed | 1 |
No direct human evidence in the Atlas for this entity yet — everything below rests on animal or molecular work.
Studies
| Year | Evidence | Study |
|---|---|---|
| 2016 | A | Cardioprotection and lifespan extension by the natural polyamine spermidine EIS2016 The mammalian follow-up to EIS2009 and the reason the spermidine branch matters for human health claims: oral spermidine extends mouse lifespan, reduces cardiac hypertrophy and preserves diastolic function, and the protection disappears in mice whose cardiomyocytes lack Atg5, which makes autophagy necessary rather than merely correlated. Boundary: the human part is a dietary questionnaire correlated with blood pressure and cardiovascular incidence, so it is observational and does not carry the causal claim the mouse data carry. |
| 2013 | A | Overexpression of Atg5 in mice activates autophagy and extends lifespan PYO2013 Mice engineered with extra copies of the autophagy gene Atg5 lived 17% longer and were leaner and more insulin-sensitive. |
| 2026 | PP | Redox activation of ATG5 licenses autophagy upon nutrient restriction SHI2026 Dietary restriction selectively oxidizes a specific, tissue-resolved set of cysteines rather than oxidizing the proteome broadly. One of the most strongly oxidized is Cys19 on the core autophagy protein ATG5; this oxidation is required for ATG5 to bind ATG10 and form the ATG5-ATG12 conjugate that lipidates LC3B and builds the autophagosome. In mice lacking this redox switch, nutrient restriction fails to trigger autophagy, causing severe tissue pathology and early death -- a single oxidized cysteine gates the autophagic response to fasting. |
Related entities
Thank you. Your answer was counted anonymously.