Autophagy is a fundamental cellular process that degrades and recycles damaged or unnecessary components to maintain internal balance. It involves the formation of double membrane vesicles called autophagosomes that engulf cytoplasmic material, including proteins, lipids and organelles, and then fuse with lysosomes where the contents are broken down and reused.

Research has shown that autophagy is crucial for adaptation to stress, especially nutrient deprivation. When cells face starvation, autophagy provides amino acids and other building blocks, supporting energy production and survival. It is also important in removing defective mitochondria and misfolded proteins, helping prevent cellular damage and inflammation.

Defects in autophagy are linked to a wide range of diseases. In neurodegenerative disorders such as Parkinson’s and Alzheimer’s disease, impaired autophagy contributes to accumulation of toxic protein aggregates. In cancer, autophagy has a dual role. It can suppress tumor formation by limiting DNA damage and chronic inflammation, but established tumors may exploit autophagy to survive in hostile environments and resist therapy.

Autophagy declines with age, which may promote the buildup of cellular damage and functional decline of tissues. Enhancing autophagy is being studied as a strategy to promote healthy aging and extend healthspan. Caloric restriction, intermittent fasting, some dietary components and certain drugs can stimulate autophagy in experimental models.

Current research focuses on mapping the molecular machinery that controls autophagy, understanding how it interacts with other cellular pathways such as metabolism and immunity, and developing safe interventions that selectively modulate autophagy in specific tissues or disease contexts.