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Cited by 107Autophagy in Disease and TherapyParkinson's Disease Mechanisms and TreatmentsHeat shock proteins research

Essential control of mitochondrial morphology and function by chaperone-mediated autophagy through degradation of PARK7

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Wang, Bao, Cai, Zhibiao, Tao, Kai, Zeng, Weijun, Lu, Fangfang, Yang, Ruixin, Feng, Dayun, Gao, Guodong +1 more·2016·Autophagy
DOI 10.1080/15548627.2016.1179401PMC PMC4968227
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Abstract

As a selective degradation system, chaperone-mediated autophagy (CMA) is essential for maintaining cellular homeostasis and survival under stress conditions. Increasing evidence points to an important role for the dysfunction of CMA in the pathogenesis of Parkinson disease (PD). However, the mechanisms by which CMA regulates neuronal survival under stress and its role in neurodegenerative diseases are not fully understood. PARK7/DJ-1 is an autosomal recessive familial PD gene. PARK7 plays a critical role in antioxidative response and its dysfunction leads to mitochondrial defects. In the current study, we showed that CMA mediated the lysosome-dependent degradation of PARK7. Importantly, CMA preferentially removed the oxidatively damaged nonfunctional PARK7 protein. Furthermore, CMA protected cells from mitochondrial toxin MPP(+)-induced changes in mitochondrial morphology and function, and increased cell viability. These protective effects were lost under PARK7-deficiency conditions. Conversely, overexpression of PARK7 significantly attenuated the mitochondrial dysfunction and cell death exacerbated by blocking CMA under oxidative stress. Thus, our findings reveal a mechanism by which CMA protects mitochondrial function by degrading nonfunctional PARK7 and maintaining its homeostasis, and dysregulation of this pathway may contribute to the neuronal stress and death in PD pathogenesis.

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  • Neurons rely heavily on local proteostasis that requires robust lysosomal trafficking and positioning due to their long axons and dendrites.

    “At a mechanistic level, the long processes of axons and dendrites mean that neurons rely heavily on local proteostasis that requires robust lysosomal trafficking and positioning.154,155”

    From The lysosome and proteostatic stress at the intersection of pediatric neurological disorders and adult neurodegenerative diseases (2025) · cites this paper as [155]

    The Introduction links disrupted protein homeostasis to neurodegeneration, and the Results section ‘Degradation of PARK7 by lysosomes’ examines lysosomal protein degradation in a dopamine-neuron progenitor cell line. Neither passage addresses local proteostasis in axons or dendrites, or a need for lysosomal trafficking and positioning because of their length; those mechanistic parts of the claim are unsupported. (LLM, conf=0.77)

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Cited by

Sorted by citations

Authors
Wang, B., Cai, Z., Tao, K., Zeng, W., Lu, F., Yang, R., Feng, D., Gao, G., & Yang, Q.
Affiliations
Tang Du Hospital (CN)
Corresponding author
  • Gao, Guodong
  • Yang, Qian
ORCID
Venue
Autophagy
Publisher
Informa UK Limited
Published
2016-06-10
Volume
12
Issue
8
Pages
1215-1228
ISSN
  • 1554-8627 (ISSN-L)
  • 1554-8635
DOI
10.1080/15548627.2016.1179401
PMC
PMC4968227
OpenAlex
W2353796718
Cited by
107
References
1
Citations by year
2026: 10 · 2025: 7 · 2024: 10 · 2023: 8 · 2022: 12 · 2021: 13 · 2020: 8 · 2019: 8 · 2018: 15 · 2017: 11 · 2016: 4 · 2012: 1
FWCI
11.88
Type
journal article
Language
en
Open access
Licence
Locations
  • Autophagy (publishedVersion, cc-by-nc)
  • Europe PMC (PubMed Central) (publishedVersion, cc-by-nc)
  • PubMed Central (publishedVersion, cc-by-nc)
  • PubMed (publishedVersion)
Topics
  • Health Sciences › Medicine › Epidemiology › Autophagy in Disease and Therapy
  • Health Sciences › Medicine › Neurology › Parkinson's Disease Mechanisms and Treatments
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Heat shock proteins research
Keywords
chaperone-mediated autophagy, DJ-1, Parkinson's disease, mitochondrial morphology, mitochondrial dysfunction, oxidative stress, MPP+, lysosomal degradation, neuronal survival, neurodegeneration, protein quality control
MeSH terms
Protein Deglycase DJ-1, Animals, Antioxidants, Autophagy, Cell Survival, Gene Expression Regulation, Homeostasis, Humans, Lysosomes, Male, Mice, Transgenic, Mitochondria, Neurons, Parkinson Disease, Cell Death, Rats, Sprague-Dawley, Oxidative Stress, Molecular Chaperones, Neurodegenerative Diseases, Amino Acid Motifs, Mice, HEK293 Cells

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