ReviewNeuroscience bulletin2015
Chaperone-mediated autophagy and neurodegeneration: connections, mechanisms, and therapeutic implications.
Review in Neuroscience bulletin, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
7 citing papers in PubMed, 19 citations in OpenAlex.
- Targeting autophagy in Alzheimer's disease: Animal models and mechanisms.Zoological research · 2023Review
- Chaperone-Mediated Autophagy and Its Implications for Neurodegeneration and Cancer.International journal of general medicine · 2022Review
- Article
- Phosphorylation of LAMP2A by p38 MAPK couples ER stress to chaperone-mediated autophagy.Nature communications · 2017Article
- Essential control of mitochondrial morphology and function by chaperone-mediated autophagy through degradation of PARK7.Autophagy · 2016Article
- Chaperone-Mediated Autophagy and Mitochondrial Homeostasis in Parkinson's Disease.Parkinson's disease · 2016Review
- Selective role of autophagy in neuronal function and neurodegenerative diseases.Neuroscience bulletin · 2015Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 4 institutions in 2 countries.
Funding
Abstract
Lysosomes degrade dysfunctional intracellular components via three pathways: macroautophagy, microautophagy, and chaperone-mediated autophagy (CMA). Unlike the other two, CMA degrades cytosolic proteins with a recognized KFERQ-like motif in lysosomes and is important for cellular homeostasis. CMA activity declines with age and is altered in neurodegenerative diseases. Its impairment leads to the accumulation of aggregated proteins, some of which may be directly tied to the pathogenic processes of neurodegenerative diseases. Its induction may accelerate the clearance of pathogenic proteins and promote cell survival, representing a potential therapeutic approach for the treatment of neurodegenerative diseases. In this review, we summarize the current findings on how CMA is involved in neurodegenerative diseases, especially in Parkinson's disease.
Indexed as
Identifiers
What OpenQuestion holds
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.