ArticleBrain and behavior2019
The role of chaperone-mediated autophagy in neurotoxicity induced by alpha-synuclein after methamphetamine exposure.
Article in Brain and behavior, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers, 1 of them a synthesis that pooled it.
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Who cites it
19 citing papers in PubMed, 1 synthesis or guideline pooled it, 32 citations in OpenAlex.
- Molecular mechanisms of programmed cell death in methamphetamine-induced neuronal damage.Frontiers in pharmacology · 2022Pooled it
- Endogenous Expression of HSP70 and Thioredoxin-1 During Methamphetamine-Induced Degeneration.Biomedicines · 2026Article
- Increase of α-Synuclein in the Peripheral Blood of Subjects with Methamphetamine Use Disorder.Psychiatry investigation · 2025Article
- Single-Cell RNA-Seq Uncovers Robust Glial Cell Transcriptional Changes in Methamphetamine-Administered Mice.International journal of molecular sciences · 2025Article
- Differentially Expressed Nedd4-binding Protein Ndfip1 Protects Neurons Against Methamphetamine-induced Neurotoxicity.Neurotoxicity research · 2025Article
- Methamphetamine Increases Tubulo-Vesicular Areas While Dissipating Proteins from Vesicles Involved in Cell Clearance.International journal of molecular sciences · 2024Article
- The Common Denominators of Parkinson's Disease Pathogenesis and Methamphetamine Abuse.Current neuropharmacology · 2024Review
- Proteinopathies: Deciphering Physiology and Mechanisms to Develop Effective Therapies for Neurodegenerative Diseases.Molecular neurobiology · 2022Review
- Neurotoxicity of methamphetamine: Main effects and mechanisms.Experimental neurology · 2021Review
- Mystery of methamphetamine-induced autophagosome accumulation in hippocampal neurons: loss of syntaxin 17 in defects of dynein-dynactin driving and autophagosome-late endosome/lysosome fusion.Archives of toxicology · 2021Article
- The Role of α-Synuclein in Methamphetamine-Induced Neurotoxicity.Neurotoxicity research · 2021Review
- Melatonin and Autophagy in Aging-Related Neurodegenerative Diseases.International journal of molecular sciences · 2020Review
- Microautophagy upregulation in cutaneous lymph nodes of dogs naturally infected by Leishmania infantum.Parasitology research · 2020Article
- Chaperones and Proteostasis: Role in Parkinson's Disease.Diseases (Basel, Switzerland) · 2020Review
- Effect of Parkin on methamphetamine-induced α-synuclein degradation dysfunction in vitro and in vivo.Brain and behavior · 2020Article
- α-synuclein promotes progression of Parkinson's disease by upregulating autophagy signaling pathway to activate NLRP3 inflammasome.Experimental and therapeutic medicine · 2020Article
- Impact of Chaperone-Mediated Autophagy in Brain Aging: Neurodegenerative Diseases and Glioblastoma.Frontiers in aging neuroscience · 2020Article
- The role of chaperone-mediated autophagy in neurotoxicity induced by alpha-synuclein after methamphetamine exposure.Brain and behavior · 2019Article
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
introductionChaperone-mediated autophagy (CMA) is an autophagy-lysosome pathway (ALP) that is different from the other two lysosomal pathways, namely, macroautophagy and microautophagy, and can selectively degrade cytosolic proteins in lysosomes without vesicle formation. CMA activity declines in neurodegenerative diseases such as Parkinson's disease, and similar neurotoxicity can occur after methamphetamine (METH) treatment. The relationship between CMA and METH-induced neurotoxicity is not clear.
methodsWe detected changes in the chaperone protein Hsc70 and the lysosomal surface receptor Lamp-2a after METH treatment and then regulated these two proteins by small interfering RNA and DNA plasmid transfection to investigate how CMA influences METH-induced neurotoxicity.
resultsWe found that CMA activity is decreased after METH exposure in neurons and downregulated Lamp-2a can aggravate the neurotoxicity induced by α-Syn after METH exposure and that Hsc70 overexpression can relieve the abnormal levels of alpha-synuclein and its aggregate forms and the increase in cell apoptosis induced by METH.
conclusionsThe results provide in vivo evidence for CMA plays a pivotal role in METH-induced neurotoxicity, and upregulation of Hsc70 expression significantly protects neuronal cells against METH-induced toxicity. This research may pave the way for potential therapeutic approaches targeting CMA for METH abuse and neurodegenerative disorders.
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