The DOI matches its Crossref record; 155 of the 157 references it cites were found in a registry or an index.
Autophagy in Neurons
Open accessAbstract
Autophagy is the major cellular pathway to degrade dysfunctional organelles and protein aggregates. Autophagy is particularly important in neurons, which are terminally differentiated cells that must last the lifetime of the organism. There are both constitutive and stress-induced pathways for autophagy in neurons, which catalyze the turnover of aged or damaged mitochondria, endoplasmic reticulum, other cellular organelles, and aggregated proteins. These pathways are required in neurodevelopment as well as in the maintenance of neuronal homeostasis. Here we review the core components of the pathway for autophagosome biogenesis, as well as the cell biology of bulk and selective autophagy in neurons. Finally, we discuss the role of autophagy in neuronal development, homeostasis, and aging and the links between deficits in autophagy and neurodegeneration.
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“Reducing tau acetylation restores its degradation through CMA (Figure 5).90,147”
From The lysosome and proteostatic stress at the intersection of pediatric neurological disorders and adult neurodegenerative diseases (2025) · cites this paper as [147]
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“Tau acetylation contributes to tau pathology via multiple potential mechanisms: promoting tau fibrillation146 and impairing tau clearance through CMA both by reducing entry into the lysosome and proteolysis by the lysosome.147”
From The lysosome and proteostatic stress at the intersection of pediatric neurological disorders and adult neurodegenerative diseases (2025) · cites this paper as [147]
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1 retracted
RETRACTED ARTICLE: Parkin and PINK1 mitigate STING-induced inflammation
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“The importance of more fully understanding mitochondrial quality control is emphasized by the observation that both PINK1 and Parkin knockout mice are susceptible to stress, and that this in turn leads to inflammation (Sliter et al. 2018).”
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“The best characterized autophagy receptor known to function in aggrephagy is p62/ SQSTM1 (Bjørkøy et al. 2005, Komatsu et al. 2007a, Pankiv et al. 2007).”
BackgroundParkin is recruited selectively to impaired mitochondria and promotes their autophagy
Narendra, D., Tanaka, A., Suen, D.-F., & Youle, R. J. (2008) · The Journal of Cell Biology · doi:10.1083/jcb.200809125 · Cited by 4,026 · cited 1×
“Work has shown that PINK1 is a mitochondrially-targeted kinase involved in the recruitment of the E3 ubiquitin ligase Parkin to impaired mitochondria (Narendra et al. 2008, 2010a).”
BackgroundSuppression of basal autophagy in neural cells causes neurodegenerative disease in mice
Hara, T., Nakamura, K., Matsui, M., Yamamoto, A., Nakahara, Y., Suzuki-Migishima, R., Yokoyama, M., Mishima, K., Saito, I., Okano, H., et al. (2006) · Nature · doi:10.1038/nature04724 · Cited by 3,882 · cited 2×
“While many questions remain, the importance of autophagy in neurons is clear, as the neuron-specific ablation of autophagy leads to neurodegeneration (Hara et al. 2006, Komatsu et al. 2006).”
BackgroundLoss of autophagy in the central nervous system causes neurodegeneration in mice
Komatsu, M., Waguri, S., Chiba, T., Murata, S., Iwata, J.-I., Tanida, I., Ueno, T., Koike, M., Uchiyama, Y., Kominami, E., et al. (2006) · Nature · doi:10.1038/nature04723 · Cited by 3,500 · cited 3×
“While many questions remain, the importance of autophagy in neurons is clear, as the neuron-specific ablation of autophagy leads to neurodegeneration (Hara et al. 2006, Komatsu et al. 2006).”
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BackgroundInfluentialPINK1 Is Selectively Stabilized on Impaired Mitochondria to Activate Parkin
Narendra, D. P., Jin, S. M., Tanaka, A., Suen, D.-F., Gautier, C. A., Shen, J., Cookson, M. R., & Youle, R. J. (2010) · PLoS Biology · doi:10.1371/journal.pbio.1000298 · Cited by 2,944
The ubiquitin kinase PINK1 recruits autophagy receptors to induce mitophagy
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“Depletion of a single receptor such as OPTN may induce a delay in mitochondrial engulfment (Moore & Holzbaur 2016) but does not block mitophagy completely (Lazarou et al. 2015), indicating some redundancy in the system.”
BackgroundA ubiquitin-like system mediates protein lipidation
Ichimura, Y., Kirisako, T., Takao, T., Satomi, Y., Shimonishi, Y., Ishihara, N., Mizushima, N., Tanida, I., Kominami, E., Ohsumi, M., et al. (2000) · Nature · doi:10.1038/35044114 · Cited by 2,139 · cited 1×
“Elongation of the autophagosome membrane is mediated by the aptly named elongation complex, composed of two ubiquitin-like conjugation complexes (Ichimura et al. 2000, Mizushima et al. 1998).”
BackgroundHomeostatic levels of p62 control cytoplasmic inclusion body formation in autophagy-deficient mice.
Komatsu, M., Waguri, S., Koike, M., Sou, Y.-S., Ueno, T., Hara, T., Mizushima, N., Iwata, J.-I., Ezaki, J., Murata, S., et al. (2007) · Cell · doi:10.1016/j.cell.2007.10.035 · Cited by 2,124 · cited 3×
“Likewise, conditionally knocking out Atg7 in Purkinje cells using the Pcp2 promoter in mice did not appear to affect dendrites, but did lead to neuronal and axonal dystrophy, degeneration of axon terminals, and eventual neuronal death (Komatsu et al. 2007b).”
Background
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de Athaide, M. M., Leal-Calvo, T., da Silva, T. P., Rosa, T. L. S. A., Ferreira, H., Pascarelli, B. M. D. O., de Sousa, A. C. S., Jardim, M., & Pinheiro, R. O. (2025) · Frontiers in Immunology · doi:10.3389/fimmu.2025.1550687
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“Basal autophagy is essential for cellular homeostasis and survival whereas loss of autophagy is detrimental to cells, particularly for post-mitotic cells like neurons.(1,6,7,20,24) Autophagy dysfunction is reported in several neurodegenerative diseases that are considered to contribute to the disease pathology.”
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Unraveling Pathophysiological Link Between Mitophagy Pathway and Vascular Dementia
Kumaş‐Kulualp, M., Kadırhan, Ö. A., & Demırci, M. (2022) · Archives of Neuroscience · doi:10.5812/ans-124588
Metadata
- Authors
- Stavoe, A. K. H., & Holzbaur, E. L. F.
- Affiliations
- University of Pennsylvania (US)
- Venue
- Annual Review of Cell and Developmental Biology
- Publisher
- Annual Reviews
- Published
- 2019-10-06
- Volume
- 35
- Issue
- 1
- Pages
- 477-500
- ISSN
- 1081-0706 (ISSN-L)
- 1530-8995
- PMC
- PMC6996145
- OpenAlex
- W2963539474
- Cited by
- 328
- References
- 157
- Citations by year
- 2026: 41 · 2025: 56 · 2024: 59 · 2023: 61 · 2022: 58 · 2021: 28 · 2020: 21 · 2019: 3
- FWCI
- 4.01
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Annual Review of Cell and Developmental Biology (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institutes of Health
- National Institute of Neurological Disorders and Stroke (K99NS109286, R37NS060698)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Autophagy in Disease and Therapy
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Ubiquitin and proteasome pathways
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Aging › Genetics, Aging, and Longevity in Model Organisms
- Keywords
- autophagy, neurons, autophagosome formation, selective autophagy, bulk autophagy, mitochondrial turnover, protein aggregation, brain development, neuronal homeostasis, aging, neurodegeneration, endoplasmic reticulum, organelle degradation
- MeSH terms
- Autophagosomes, Animals, Autophagy, Axons, Dendrites, Endoplasmic Reticulum, Homeostasis, Humans, Memory, Mitochondria, Neurons, Synapses, Neurodegenerative Diseases, Proteasome Endopeptidase Complex, Ubiquitination, Unfolded Protein Response
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