ReviewBritish journal of pharmacology2014
Quality control gone wrong: mitochondria, lysosomal storage disorders and neurodegeneration.
Review in British journal of pharmacology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.
What it found
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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.
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
45 citing papers in PubMed, 75 citations in OpenAlex.
- Cellular Organelle-Related Transcriptomic Profile Abnormalities in Neuronopathic Types of Mucopolysaccharidosis: A Comparison with Other Neurodegenerative Diseases.Current issues in molecular biology · 2024Article
- Improving lysosomal ferroptosis with NMN administration protects against heart failure.Life science alliance · 2023Article
- Article
- Expert-opinion-based guidance for the care of children with lysosomal storage diseases during the COVID-19 pandemic: An experience-based Turkey perspective.Frontiers in public health · 2023Review
- Genetics of BAG3: A Paradigm for Developing Precision Therapies for Dilated Cardiomyopathies.Journal of the American Heart Association · 2022Review
- Neuronopathic Gaucher disease: Beyond lysosomal dysfunction.Frontiers in molecular neuroscience · 2022Review
- Mitophagy: An Emergence of New Player in Alzheimer's Disease.Frontiers in molecular neuroscience · 2022Review
- Modulation of Autophagy Through Regulation of 5'-AMP-Activated Protein Kinase Affects Mitophagy and Mitochondrial Function in Primary Human Trophoblasts.Reproductive sciences (Thousand Oaks, Calif.) · 2021Article
- Exercise Training Improves Memory Performance in Older Adults: A Narrative Review of Evidence and Possible Mechanisms.Frontiers in human neuroscience · 2021Review
- Characterization of New Proteomic Biomarker Candidates in Mucopolysaccharidosis Type IVA.International journal of molecular sciences · 2020Article
- Decreased Mitochondrial Function, Biogenesis, and Degradation in Peripheral Blood Mononuclear Cells from Amyotrophic Lateral Sclerosis Patients as a Potential Tool for Biomarker Research.Molecular neurobiology · 2020Article
- Lysosomal Storage Disorders Shed Light on Lysosomal Dysfunction in Parkinson's Disease.International journal of molecular sciences · 2020Review
- LRRK2 and α-Synuclein: Distinct or Synergistic Players in Parkinson's Disease?Frontiers in neuroscience · 2020Review
- Exercise activates lysosomal function in the brain through AMPK-SIRT1-TFEB pathway.CNS neuroscience & therapeutics · 2019Article
- Trehalose as a promising therapeutic candidate for the treatment of Parkinson's disease.British journal of pharmacology · 2019Review
- Is autophagy an elective strategy to protect neurons from dysregulated cholesterol metabolism?Neural regeneration research · 2019Review
- Impaired autophagic and mitochondrial functions are partially restored by ERT in Gaucher and Fabry diseases.PloS one · 2019Article
- Alpha-synuclein fibrils recruit TBK1 and OPTN to lysosomal damage sites and induce autophagy in microglial cells.Journal of cell science · 2018Article
- Neuromuscular degeneration and locomotor deficit in aDisease models & mechanisms · 2018Article
- Small molecule natural compound agonist of SIRT3 as a therapeutic target for the treatment of intervertebral disc degeneration.Experimental & molecular medicine · 2018Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 2 institutions in 1 country.
Funding
Abstract
The eukaryotic cell possesses specialized pathways to turn over and degrade redundant proteins and organelles. Each pathway is unique and responsible for degradation of distinctive cytosolic material. The ubiquitin-proteasome system and autophagy (chaperone-mediated, macro, micro and organelle specific) act synergistically to maintain proteostasis. Defects in this equilibrium can be deleterious at cellular and organism level, giving rise to various disease states. Dysfunction of quality control pathways are implicated in neurodegenerative diseases and appear particularly important in Parkinson's disease and the lysosomal storage disorders. Neurodegeneration resulting from impaired degradation of ubiquitinated proteins and α-synuclein is often accompanied by mitochondrial dysfunction. Mitochondria have evolved to control a diverse number of processes, including cellular energy production, calcium signalling and apoptosis, and like every other organelle within the cell, they must be 'recycled.' Failure to do so is potentially lethal as these once indispensible organelles become destructive, leaking reactive oxygen species and activating the intrinsic cell death pathway. This process is paramount in neurons which have an absolute dependence on mitochondrial oxidative phosphorylation as they cannot up-regulate glycolysis. As such, mitochondrial bioenergetic failure can underpin neural death and neurodegenerative disease. In this review, we discuss the links between cellular quality control and neurodegenerative diseases associated with mitochondrial dysfunction, with particular attention to the emerging links between Parkinson's and Gaucher diseases in which defective quality control is a defining factor.
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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.