Abstract
Autophagy is a conserved catabolic process critical for cell homeostasis with broad implications for aging and age-associated diseases. A defining feature of autophagy is the de novo formation of a specialized transient organelle, the double-membrane autophagosome. Autophagosomes originate from small vesicular precursors after rapid membrane expansion resulting in the engulfment of a broad spectrum of cytoplasmic cargoes within a few minutes for vacuolar or lysosomal degradation. Recent advances have provided exciting new insights into the molecular mechanisms underlying the assembly of autophagic membranes during autophagosome biogenesis. Specifically, the phospholipid biosynthesis activity of the endoplasmic reticulum and a dedicated membrane-tethering complex between nascent autophagosomes and the endoplasmic reticulum have emerged as key factors in autophagosome formation.
Highlights
Autophagy is a conserved catabolic process critical for cell homeostasis with broad implications for aging and age-associated diseases
Consistent with its central role, it has become clear that defects in autophagy are linked to aging and a broad spectrum of common age-associated diseases, including neurodegeneration, diabetes, and cancer[2,3,4]
The exceptional degradative capacity of autophagy is based on the formation of a specialized transient organelle, termed autophagosome, that surrounds and isolates substrates from the rest of the cytoplasm within a characteristic double-membrane structure
Summary
Autophagy is a conserved catabolic process critical for cell homeostasis with broad implications for aging and age-associated diseases. They are commissioned and are peer reviewed before publication to ensure that the final, published version is comprehensive and accessible.
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