ReviewFrontiers in molecular neuroscience2016
Role of Chaperone-Mediated Autophagy Dysfunctions in the Pathogenesis of Parkinson's Disease.
Review in Frontiers in molecular neuroscience, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
52 citing papers in PubMed, 74 citations in OpenAlex.
- G3BP1 depletion, observed in Parkinson's Disease, drives Golgi-lysosome-autophagy defects.Cell death and differentiation · 2026Article
- Starvation-induced HSC70 O-GlcNAcylation activates chaperone-mediated autophagy.The Journal of biological chemistry · 2026Article
- The Expanding Role of Non-Coding RNAs in Neurodegenerative Diseases: From Biomarkers to Therapeutic Targets.Pharmaceuticals (Basel, Switzerland) · 2026Review
- Autophagy-lysosomal pathway in neurodegeneration.Molecular neurodegeneration advances · 2026Review
- Research progress on the α-synuclein-lysosome axis in Parkinson's disease: molecular mechanisms of protein aggregation, autophagy dysfunction, and therapeutic targeting.Frontiers in neuroscience · 2026Review
- α-Synuclein Pathology in Synucleinopathies: Mechanisms, Biomarkers, and Therapeutic Challenges.International journal of molecular sciences · 2025Review
- BAG3's dual roles in Parkinson's disease and cardiomyopathy: benefit or liability?Acta neuropathologica · 2024Article
- The role of polo-like kinases 2 in the proteasomal and lysosomal degradation of alpha-synuclein in neurons.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2024Article
- Navigating the Neurobiology of Parkinson's: The Impact and Potential of α-Synuclein.Biomedicines · 2024Review
- Review
- VPS35 and retromer dysfunction in Parkinson's disease.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2024Review
- Pathophysiology of COVID-19-Related Extrapyramidal Disorders.Advances in experimental medicine and biology · 2024Review
- The post-translational regulation of transcription factor EB (TFEB) in health and disease.EMBO reports · 2023Review
- Iron-inhibited autophagy via transcription factor ZFP27 in Parkinson's disease.Journal of cellular and molecular medicine · 2023Article
- LAMP2A, LAMP2B and LAMP2C: similar structures, divergent roles.Autophagy · 2023Review
- Chaperone-mediated autophagy in neurodegenerative diseases: mechanisms and therapy.Molecular and cellular biochemistry · 2023Review
- Inhibiting mitochondrial fission rescues degeneration in hereditary spastic paraplegia neurons.Brain : a journal of neurology · 2022Article
- Autophagy and Its Association with Genetic Mutations in Parkinson Disease.Medical science monitor : international medical journal of experimental and clinical research · 2022Review
- Understanding the contributions of VPS35 and the retromer in neurodegenerative disease.Neurobiology of disease · 2022Review
- Extracellular vesicle miR-32 derived from macrophage promotes arterial calcification in mice with type 2 diabetes via inhibiting VSMC autophagy.Journal of translational medicine · 2022Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Chaperone-mediated autophagy (CMA) represents a selective form of autophagy involved in the degradation of specific soluble proteins containing a pentapeptide motif that is recognized by a cytosolic chaperone able to deliver proteins to the lysosomes for degradation. Physiologically, CMA contributes to maintain crucial cellular functions including energetic balance and protein quality control. Dysfunctions in CMA have been associated to the pathogenesis of several neurodegenerative diseases characterized by accumulation and aggregation of proteins identified as CMA substrates. In particular, increasing evidence highlights the existence of a strong relationship between CMA defects and Parkinson's disease (PD). Several mutations associated with familial forms of PD (SNCA, LRRK2, UCHL1 and DJ-1) have been demonstrated to block or reduce the activity of CMA, the main catabolic pathway for alpha-synuclein (asyn). CMA dysfunctions also leads to a mislocalization and inactivation of the transcription factor MEF2D that plays a key-role in the survival of dopaminergic neurons. Furthermore, reduced levels of CMA markers have been observed in post mortem brain samples from PD patients. The aim of this review article is to provide an organic revision of evidence for the involvement of CMA dysfunctions in the pathogenesis of PD. Updated findings obtained in patient's specimens will be resumed, and results deriving from
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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.