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Autophagy

Autophagy

Autophagy is a self-digesting process by which a cell protects itself from threats both within and outside the cell, ranging from abnormal proteins to invading bacteria. In this process, obsolete components of the cell and invading microbes are degraded by hydrolytic enzymes active in an acidic environment of the lysosomal lumen.
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Related Experiment Video

Updated: Dec 17, 2025

Exploring the Regulation of Lipid Droplet Catabolism through Lipophagy

Exploring the Regulation of Lipid Droplet Catabolism through Lipophagy

Published on: January 31, 2025

Liquid-liquid phase separation in autophagy.

Nobuo N Noda¹, Zheng Wang², Hong Zhang^2,3

¹Institute of Microbial Chemistry (BIKAKEN), Tokyo, Japan.

The Journal of Cell Biology

|July 1, 2020

Summary

Liquid-liquid phase separation (LLPS) drives autophagy by forming dynamic condensates. Aberrant LLPS under stress can impair cellular cleanup, highlighting targets for protein aggregation diseases.

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Last Updated: Dec 17, 2025

Exploring the Regulation of Lipid Droplet Catabolism through Lipophagy

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Ultrastructural Localization of Endogenous LC3 by On-Section Correlative Light-Electron Microscopy

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Live Cell Imaging of Early Autophagy Events: Omegasomes and Beyond

Live Cell Imaging of Early Autophagy Events: Omegasomes and Beyond

Published on: July 27, 2013

Area of Science:

Biochemistry
Cell Biology
Molecular Biology

Background:

Liquid-liquid phase separation (LLPS) is crucial for organizing cellular components into distinct condensates.
These condensates can transition between liquid, gel, and solid states, impacting their function.
LLPS is implicated in key stages of autophagy, including autophagosome formation and cargo triage.

Purpose of the Study:

To elucidate the role of LLPS in autophagy.
To investigate the functional implications of condensate state transitions in autophagy.
To explore how aberrant phase separation under stress affects autophagy and disease.

Main Methods:

The study reviews existing literature on LLPS and autophagy.
It analyzes the mechanisms of condensate formation, transition, and their regulation.
It discusses the impact of stress and disease on these processes.

Main Results:

LLPS mediates autophagosome biogenesis and protein degradation pathways.
Gel-like condensates, not solid ones, are shown to initiate autophagosome membrane formation.
Dysregulated phase separation in pathological conditions can evade cellular surveillance mechanisms.

Conclusions:

LLPS is a fundamental process in autophagy, with condensate dynamics dictating function.
Aberrant phase separation contributes to disease pathogenesis by disrupting cellular quality control.
Targeting LLPS mechanisms offers potential therapeutic strategies for protein aggregation disorders.