Role of autophagy in cell survival and death: Mechanisms and therapeutic implications.

Autophagy is a catabolic process that preserves cellular homeostasis by degrading and recycling damaged organelles and proteins, particularly during metabolic stress, nutrient deprivation, oxidative stress, and inflammation. It is tightly regulated by key molecular pathways, including AMP-activated protein kinase (AMPK) and mammalian target of rapamycin (mTOR). Core autophagy-related proteins such as Unc-51-like kinase 1 (ULK1), autophagy-related genes (ATG4, ATG5, ATG7), and microtubule-associated protein 1 light chain 3 (LC3), orchestrate autophagosome formation and cargo degradation. Autophagy influences cellular fate, promoting survival or programmed cell death, and plays a critical role in stem cell differentiation. Impaired autophagy contributes to neurodegenerative diseases by enabling toxic protein accumulation, while its dysregulation affects lipid metabolism and insulin sensitivity in metabolic syndromes and cancers. This chapter explores the molecular mechanisms of autophagy, its regulatory networks, and its implications in disease, emphasizing potential therapeutic interventions. Understanding these pathways provides insights into novel strategies for targeting autophagy in various pathological conditions.