The DOI matches its Crossref record; 127 of the 127 references it cites were found in a registry or an index.
The Autophagy–Lysosomal Pathway in Neurodegeneration: A TFEB Perspective
Open accessAbstract
The autophagy-lysosomal pathway (ALP) is involved in the degradation of long-lived proteins. Deficits in the ALP result in protein aggregation, the generation of toxic protein species, and accumulation of dysfunctional organelles, which are hallmarks of Alzheimer's disease (AD), Parkinson's disease (PD), Huntington's disease (HD), and prion disease. Decades of research have therefore focused on enhancing the ALP in neurodegenerative diseases. More recently, transcription factor EB (TFEB), a major regulator of autophagy and lysosomal biogenesis, has emerged as a leading factor in addressing disease pathology. We review the regulation of the ALP and TFEB and their impact on neurodegenerative diseases. We also offer our perspective on the complex role of autophagy and TFEB in disease pathogenesis and its therapeutic implications through the examination of prion disease.
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“TFE3 or TFEB upregulation or activation through pharmacological inhibition of mTORC1 can trigger clearance of excess α-synuclein and halt the progression of neurotoxicity17–22.”
From PDCD4 triggers α-synuclein accumulation and motor deficits via co-suppressing TFE3 and TFEB translation in a model of Parkinson’s disease (2024) · cites this paper as [20]
Experimental — accuracy not yet measuredIn the citing paper
“Molecular and histopathologic analyses of patient tissues demonstrate mislocalized or accumulated autophagy machinery, pathogenic mutations underlying familial neurodegenerative diseases disable known autophagy-related factors, and genetically ablating autophagy effectors produce neurodegeneration in cell and animal model systems [74–81], supporting a role for autophagy dysfunction in the devel”
From Autophagy and ALS: mechanistic insights and therapeutic implications (2022) · cites this paper as [79]
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Cites
Repertoires of Autophagy in the Pathogenesis of Ocular Diseases
Li, Y., Jiang, Q. L., Cao, G.-F., Yao, J., & Yan, B. (2015) · Cellular Physiology and Biochemistry · doi:10.1159/000373980 · Cited by 16,351
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mTOR: from growth signal integration to cancer, diabetes and ageing
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Suppression of basal autophagy in neural cells causes neurodegenerative disease in mice
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Bcl-2 Antiapoptotic Proteins Inhibit Beclin 1-Dependent Autophagy
Pattingre, S., Tassa, A., Qu, X., Garuti, R., Liang, X. H., Mizushima, N., Packer, M., Schneider, M. D., & Levine, B. (2005) · Cell · doi:10.1016/j.cell.2005.07.002 · Cited by 3,536
Loss 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
TFEB Links Autophagy to Lysosomal Biogenesis
Settembre, C., Di Malta, C., Polito, V. A., Arencibia, M. G., Vetrini, F., Erdin, S., Erdin, S. U., Huynh, T., Medina, D., Colella, P., et al. (2011) · Science · doi:10.1126/science.1204592 · Cited by 3,365
Self-citationThe Role of Atg Proteins in Autophagosome Formation
Mizushima, N., Yoshimori, T., & Ohsumi, Y. (2011) · Annual Review of Cell and Developmental Biology · doi:10.1146/annurev-cellbio-092910-154005 · Cited by 2,978
The ubiquitin kinase PINK1 recruits autophagy receptors to induce mitophagy
Lazarou, M., Sliter, D. A., Kane, L. A., Sarraf, S. A., Wang, C., Burman, J. L., Sideris, D. P., Fogel, A. I., & Youle, R. J. (2015) · Nature · doi:10.1038/nature14893 · Cited by 2,774
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Lysosomes as dynamic regulators of cell and organismal homeostasis
Ballabio, A., & Bonifacino, J. S. (2020) · Nature Reviews Molecular Cell Biology · doi:10.1038/s41580-019-0185-4 · Cited by 1,469
Self-citationTargeted protein degradation: mechanisms, strategies and application
Zhao, L., Zhao, J., Zhong, K., Tong, A., & Jia, D. (2022) · Signal Transduction and Targeted Therapy · doi:10.1038/s41392-022-00966-4 · Cited by 1,035
Lysosomes as a therapeutic target
Bonam, S. R., Wang, F., & Muller, S. (2019) · Nature Reviews Drug Discovery · doi:10.1038/s41573-019-0036-1 · Cited by 786
“TFEB has received particular attention in this regard [193] [194] [195] , with recent data suggesting that TFEB is selectively lost in patients with AD (as well as ALS) 196 .”
BackgroundAutophagy: The spotlight for cellular stress responses
Ravanan, P., Florance, I., & Talwar, P. (2017) · Life Sciences · doi:10.1016/j.lfs.2017.08.029 · Cited by 595
Nixon, R. A. (2017) · The FASEB Journal · doi:10.1096/fj.201700359 · Cited by 400
Metadata
- Authors
- Martini-Stoica, H., Xu, Y., Ballabio, A., & Zheng, H.
- Affiliations
- Baylor College of Medicine (US)
- Corresponding author
- Zheng, Hui
- Venue
- Trends in Neurosciences
- Publisher
- Elsevier BV
- Published
- 2016-04
- Volume
- 39
- Issue
- 4
- Pages
- 221-234
- ISSN
- 0166-2236 (ISSN-L)
- PMC
- PMC4928589
- OpenAlex
- W2293027573
- Cited by
- 436
- References
- 127
- Citations by year
- 2026: 38 · 2025: 41 · 2024: 46 · 2023: 65 · 2022: 48 · 2021: 53 · 2020: 43 · 2019: 34 · 2018: 27 · 2017: 31 · 2016: 10
- FWCI
- 4.61
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Trends in Neurosciences (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institutes of Health
- National Institute on Aging (RF1AG020670, F30AG050412, R01AG020670)
- National Institute of Neurological Disorders and Stroke (R01NS076117, RF1NS093652, R01NS078072, R01NS093652)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Autophagy in Disease and Therapy
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Physiology › Calcium signaling and nucleotide metabolism
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Alzheimer's disease research and treatments
- Keywords
- autophagy-lysosome pathway, TFEB, neurodegenerative diseases, lysosomal biogenesis, protein aggregation, Alzheimer's disease, Parkinson's disease, Huntington's disease, prion disease, autophagy regulation, therapeutic target
- MeSH terms
- Animals, Autophagy, Brain, Humans, Lysosomes, Nerve Degeneration, Neurodegenerative Diseases, Basic Helix-Loop-Helix Leucine Zipper Transcription Factors
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