In short
Autophagy (literally "self-eating") is the cellular process of enclosing damaged proteins and organelles in a membrane and breaking them down in the lysosome so their components can be reused.
Every cell continuously generates damaged or misfolded proteins and worn-out organelles like mitochondria. Autophagy is the disposal and recycling system for this debris: a double-membrane structure called an autophagosome forms around the targeted material, then fuses with a lysosome, whose enzymes break the contents down into amino acids, fatty acids, and other building blocks the cell can reuse. Yoshinori Ohsumi won the 2016 Nobel Prize in Physiology or Medicine for identifying the genes that control this process in yeast.
Autophagy is regulated by nutrient-sensing pathways — it is suppressed when mTOR signaling is high (abundant nutrients, growth signals) and activated when mTOR is low or AMPK is high (fasting, energy stress, exercise). This is why autophagy is often discussed alongside caloric restriction and intermittent fasting: reduced nutrient availability is one of the most reliable physiological triggers for it.
Autophagy itself is a cellular mechanism, not an intervention, so there is no single human trial that measures "autophagy" as an outcome in the way a drug trial measures blood pressure. What is separately documented in humans is that fasting and caloric restriction change the biomarkers used as proxies for autophagic activity, and that impaired autophagy is associated with age-related diseases in animal models. The link between autophagy and human lifespan extension remains inferred from that broader body of work, not established by a direct human trial.
Worth remembering
- Cells' recycling system: damaged proteins and organelles are broken down and reused.
- Suppressed by mTOR, activated by AMPK and fasting/nutrient scarcity.
- A mechanism, not an intervention — no direct human trial measures autophagy as an outcome.