Autophagy

Biological process · 17 studies in the Atlas

Cellular recycling process suppressed by mTORC1 and activated upon its inhibition; linked to longevity.

Evidence at a glance

TierWhat it meansStudies
CAnimal in vivo9
DMechanistic / in vitro / review8

No direct human evidence in the Atlas for this entity yet — everything below rests on animal or mechanistic work.

Studies

StudyYearTierFinding
LIS20262026CNotoginsenoside R1 alleviates acetaminophen-induced acute liver injury by activating protective autophagy through MAPK/mTOR pathway modulation, reducing hepatocyte death and oxidative damage.
SONH20262026CUrolithin A ameliorates HFpEF cardiac remodeling in mice by activating AMPK and inhibiting mTOR to restore mitophagic flux, while simultaneously remodeling the gut microbiome-ceramide axis to reduce l
VER20262026CTestosterone propionate protects against CCl4-induced liver fibrosis by maintaining mTOR-regulated autophagic flux via the LC3B/p62/Beclin-1 axis, preserving mitochondrial integrity; castration worsen
PYO20132013CMice engineered with extra copies of the autophagy gene Atg5 lived 17% longer and were leaner and more insulin-sensitive.
BJE20102010CFeeding rapamycin extended fly lifespan through autophagy and reduced translation, and worked even in flies already on a lifespan-maximizing diet.
CAC20102010CRevealed a vicious cycle: amyloid-beta RAISES mTOR activity, and high mTOR in turn blocks the autophagy needed to clear amyloid and tau - so the disease feeds itself. Rapamycin broke the loop in 3xTg-
SPI20102010CConnected the longevity drug to a specific age-related disease. Long-term rapamycin prevented memory deficits and lowered toxic amyloid-beta in an Alzheimer's mouse model - and the benefit tracked wit
RAV20042004CRapamycin-induced autophagy cleared toxic clumped proteins and improved symptoms in fly and mouse models of Huntington's disease.
MEL20032003CWorms lacking the autophagy gene bec-1 lost the lifespan-extending benefit of reduced insulin-like signaling - autophagy is mechanistically required for longevity, not just correlated.
BO20262026DGambogic acid exerts anti-tumor activity in lung cancer cells primarily by targeting and inhibiting mTOR signaling, demonstrated through integrated computational docking and in vitro experimental vali
JOS20242024DmTORC1 activity oscillates across the cell cycle (lowest in mitosis/G1, highest in S/G2) via the TSC complex, independent of Akt/Mek-Erk; low mTORC1 in G1 sensitizes cells to autophagy induction from
LIU20202020DThe flagship modern review of the whole field, from Sabatini's own lab (Nature Reviews Molecular Cell Biology). Maps 25+ years of mTOR biology - how it senses nutrients, controls growth and autophagy,
MAR20122012DPinned down the direct mTORC1-TFEB link: mTORC1 (docked at the lysosome via Ragulator) phosphorylates TFEB on Ser211, which traps it in the cytosol via 14-3-3 proteins. Inhibit mTORC1 and TFEB rushes
KIM20112011DRevealed the tug-of-war over ULK1: the energy sensor AMPK phosphorylates ULK1 at activating sites to turn autophagy ON when energy is low, while mTORC1 phosphorylates a different site (Ser757) to keep
LOF20112011DULK1 phosphorylates and inhibits AMPK in return, showing autophagy signaling is a bidirectional feedback loop, not a one-way switch.
SET20112011DEstablished TFEB as the single master switch that coordinates the WHOLE recycling program - it turns on both autophagosome and lysosome genes at once during starvation. This is the transcription facto
HOS20092009DShowed the DIRECT brake mTORC1 uses on autophagy: when nutrients are plentiful, mTORC1 physically joins the ULK1-Atg13-FIP200 complex (the autophagy-starter kinase) and phosphorylates ULK1 to keep it

Related entities

mTORC1 10mTOR 5Longevity 4ULK1 4Rapamycin 3AMPK 3Alzheimer's disease 2TFEB 2mTORC2 1Ragulator 1Tuberous sclerosis complex 1Huntington's disease 1

Open in the Atlas explorer