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Autophagy modulation as a potential therapeutic target for diverse diseases

David C. Rubinsztein, Patrice Codogno, Beth Levine

Nature Reviews Drug Discovery · 2012 · ▲ 1,437 citations

Abstract

The lysosomal degradation pathway known as autophagy(definition) has an essential homeostatic role in controlling the quality of the cytoplasm. However, this pathway has also been implicated in the pathology of an array of human disorders. Here, Rubinsztein and colleagues provide an overview of the mechanisms and regulation of autophagy, discuss the role of this pathway in disease and highlight potential strategies for therapeutic modulation. Autophagy is an essential, conserved lysosomal degradation pathway that controls the quality of the cytoplasm by eliminating protein aggregates and damaged organelles. It begins when double-membraned autophagosomes engulf portions of the cytoplasm, which is followed by fusion of these vesicles with lysosomes and degradation of the autophagic contents. In addition to its vital homeostatic role, this degradation pathway is involved in various human disorders, including metabolic conditions, neurodegenerative diseases, cancers and infectious diseases. This article provides an overview of the mechanisms and regulation of autophagy, the role of this pathway in disease and strategies for therapeutic modulation.

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OpenAlex
DOI
10.1038/nrd3802
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2026-08-02 MST

Cite this

APA
Rubinsztein, D.C., Codogno, P., &amp; Levine, B. (2012). Autophagy modulation as a potential therapeutic target for diverse diseases. <em>Nature Reviews Drug Discovery</em>. https://doi.org/10.1038/nrd3802
Vancouver
Rubinsztein DC, Codogno P, Levine B. Autophagy modulation as a potential therapeutic target for diverse diseases. Nature Reviews Drug Discovery. 2012. doi:10.1038/nrd3802.
BibTeX
@article{david2012Autoph, title = {Autophagy modulation as a potential therapeutic target for diverse diseases}, author = {David C. Rubinsztein and Patrice Codogno and Beth Levine}, journal = {Nature Reviews Drug Discovery}, year = {2012}, doi = {10.1038/nrd3802}, }

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