ReviewCells2022
Chaperone-Mediated Autophagy in Neurodegenerative Diseases and Acute Neurological Insults in the Central Nervous System.
Review in Cells, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
23 citing papers in PubMed, 41 citations in OpenAlex.
- The role of autophagy in spinal cord injury: Mechanisms, crosstalk, and therapeutic strategies.Neural regeneration research · 2026Article
- Huntingtin knockdown dysregulates autophagic degradation of Apolipoprotein E.Journal of Huntington's disease · 2026Article
- Potential effect of endothelial progenitor cells on pentylenetetrazole-induced seizures in rats: an evaluation of relevant lncRNAs.Journal of Zhejiang University. Science. B · 2025Article
- Sex-specific and cell-type-specific changes in chaperone-mediated autophagy across tissues during aging.Nature aging · 2025Article
- αAsarone alleviates neuronal injury by facilitating autophagy via miR-499-5p/PDCD4/ATG5 signaling pathway in ischemia stroke.Frontiers in pharmacology · 2025Article
- Treatment of Stroke at a Delayed Timepoint with a Repurposed Drug Targeting Sigma 1 Receptors.Translational stroke research · 2024Article
- Decoding Neurodegeneration: A Review of Molecular Mechanisms and Therapeutic Advances in Alzheimer's, Parkinson's, and ALS.International journal of molecular sciences · 2024Review
- The Interplay between Autophagy and Mitochondria in Cancer.International journal of molecular sciences · 2024Review
- Huntingtin contains an ubiquitin-binding domain and regulates lysosomal targeting of mitochondrial and RNA-binding proteins.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Sensitivity of substrate translocation in chaperone-mediated autophagy to Alzheimer's disease progression.Aging · 2024Article
- Endoplasmic reticulum stress and the unfolded protein response: emerging regulators in progression of traumatic brain injury.Cell death & disease · 2024Review
- Identification of a novel aromatic-turmerone analog that activates chaperone-mediated autophagy through the persistent activation of p38.Frontiers in cell and developmental biology · 2024Article
- Modulating Stress Proteins in Response to Therapeutic Interventions for Parkinson's Disease.International journal of molecular sciences · 2023Review
- Autophagy and its consequences for platelet biology.Thrombosis research · 2023Review
- Neurodegenerative Proteinopathies Induced by Environmental Pollutants: Heat Shock Proteins and Proteasome as Promising Therapeutic Tools.Pharmaceutics · 2023Review
- Pathological (Dis)Similarities in Neuronal Exosome-Derived Synaptic and Organellar Marker Levels Between Alzheimer's Disease and Frontotemporal Dementia.Journal of Alzheimer's disease : JAD · 2023Article
- Effects of retinoic acid receptor α modulators on developmental ethanol-induced neurodegeneration and neuroinflammation.Frontiers in neuroscience · 2023Article
- Novel Autophagy-Related Blood Biomarkers Associated with Immune Cell Infiltration in Ankylosing Spondylitis.Pharmacogenomics and personalized medicine · 2023Article
- Peroxiredoxin 2 Ameliorates AβO-Mediated Autophagy by Inhibiting ROS via the ROS-NRF2-p62 Pathway in N2a-APP Swedish Cells.Antioxidants (Basel, Switzerland) · 2022Article
- Brain Neurons during Physiological Aging: Morphological Features, Autophagic and Mitochondrial Contribution.International journal of molecular sciences · 2022Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Autophagy is an important function that mediates the degradation of intracellular proteins and organelles. Chaperone-mediated autophagy (CMA) degrades selected proteins and has a crucial role in cellular proteostasis under various physiological and pathological conditions. CMA dysfunction leads to the accumulation of toxic protein aggregates in the central nervous system (CNS) and is involved in the pathogenic process of neurodegenerative diseases, including Parkinson's disease and Alzheimer's disease. Previous studies have suggested that the activation of CMA to degrade aberrant proteins can provide a neuroprotective effect in the CNS. Recent studies have shown that CMA activity is upregulated in damaged neural tissue following acute neurological insults, such as cerebral infarction, traumatic brain injury, and spinal cord injury. It has been also suggested that various protein degradation mechanisms are important for removing toxic aberrant proteins associated with secondary damage after acute neurological insults in the CNS. Therefore, enhancing the CMA pathway may induce neuroprotective effects not only in neurogenerative diseases but also in acute neurological insults. We herein review current knowledge concerning the biological mechanisms involved in CMA and highlight the role of CMA in neurodegenerative diseases and acute neurological insults. We also discuss the possibility of developing CMA-targeted therapeutic strategies for effective treatments.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.