Abstract

Autophagy, an evolutionarily conserved cellular process, intricately regulates the degradation and recycling of
cellular components, ensuring cellular homeostasis. The molecular orchestration of autophagy involves a
sophisticated network of signaling pathways and key molecular players. Key initiation steps involve nutrient-sensing
pathways, including mTOR and AMPK, converging on the ULK1 complex, triggering autophagosome formation.
Subsequent stages encompass the role of the PI3K complex, recruitment of ATGs, and autophagosome expansion,
leading to cargo recognition and closure. The selectivity in autophagy is achieved through cargo-specific adaptors
and receptors like p62/SQSTM1, NIX/BNIP3L, and NDP52, ensuring targeted degradation of damaged organelles,
misfolded proteins, and pathogens. Upon fusion with lysosomes, autolysosomes are formed, culminating in the
breakdown of engulfed cargo via lysosomal hydrolases. Autophagy's intricate interplay with cellular processes,
including metabolism, immunity, and cell death pathways, underscores its multifaceted roles in physiological and
pathological conditions. Dysregulated autophagy is implicated in neurodegenerative disorders, cancer, metabolic
diseases, and infections, highlighting its clinical relevance. Understanding the molecular mechanisms of autophagy
offers promising prospects for therapeutic interventions by targeting autophagic pathways. This overview provides
insights into the molecular intricacies of autophagy, offering potential avenues for therapeutic modulation in various
disease contexts.
Keywords: Autophagy, Molecular Mechanisms, Signaling Pathways, Selective Autophagy, Lysosomal Degradation,
Cellular Homeostasis, Therapeutic Targets, Disease Implications.