Autophagy: cellular and molecular mechanisms
2010/02/03 by Danielle Glick, D.R. Glick, Sandra Barth +1 · 3,799 citations
Biochemistry, Genetics and Molecular Biology · Medicine · #ATG16L1 #Apoptosis #Autophagy #Autophagy in Disease and Therapy #Biochemistry #Biology #Calcium signaling and nucleotide metabolism #Cell biology #Disease #Endoplasmic reticulum #Extracellular vesicles in disease #Intracellular #Medicine #Mitochondrion #Mitophagy #Neurodegeneration #Organelle #Programmed cell death #Proteostasis
paper · open access · doi:10.1002/path.2697
published in The Journal of Pathology 221(1), 3-12
openalex publication_date 2010/02/03 · openalex created_date 2025/10/10 · openalex updated_date 2026/08/05
Abstract
Autophagy is a self-degradative process that is important for balancing sources of energy at critical times in development and in response to nutrient stress. Autophagy also plays a housekeeping role in removing misfolded or aggregated proteins, clearing damaged organelles, such as mitochondria, endoplasmic reticulum and peroxisomes, as well as eliminating intracellular pathogens. Thus, autophagy is generally thought of as a survival mechanism, although its deregulation has been linked to non-apoptotic cell death. Autophagy can be either non-selective or selective in the removal of specific organelles, ribosomes and protein aggregates, although the mechanisms regulating aspects of selective autophagy are not fully worked out. In addition to elimination of intracellular aggregates and damaged organelles, autophagy promotes cellular senescence and cell surface antigen presentation, protects against genome instability and prevents necrosis, giving it a key role in preventing diseases such as cancer, neurodegeneration, cardiomyopathy, diabetes, liver disease, autoimmune diseases and infections. This review summarizes the most up-to-date findings on how autophagy is executed and regulated at the molecular level and how its disruption can lead to disease.
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