ReviewFree radical biology & medicine2016
Mitochondrial control of cell bioenergetics in Parkinson's disease.
Review in Free radical biology & medicine, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 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
51 citing papers in PubMed, 86 citations in OpenAlex.
- Understanding Neurodegenerative Diseases From the -Omics Perspective: Lessons Learnt.Annals of neurology · 2026Review
- Bioenergetic and protein processing imbalances in iPSC-dopamine neurons from individuals with idiopathic Parkinson's disease.Neurobiology of disease · 2026Article
- Unlocking extracellular mitochondria from bench to clinical application in stroke.Stem cells translational medicine · 2025Review
- Metabolic Dysregulation in Parkinson's Disease: Non-Oxidative Phosphorylation and Its Role in Brain Energy Metabolism.Aging and disease · 2025Review
- Mitochondrial Dysfunction in Parkinson's Disease: A Contribution to Cognitive Impairment?International journal of molecular sciences · 2024Review
- Mitochondrial Dysfunction as a Potential Mechanism Mediating Cardiac Comorbidities in Parkinson's Disease.International journal of molecular sciences · 2024Review
- Oral Administration of Silybin Protects Against MPTP-Induced Neurotoxicity by Reducing Pro-inflammatory Cytokines and Preserving BDNF Levels in Mice.Molecular neurobiology · 2023Article
- O-GlcNAcylation is essential for therapeutic mitochondrial transplantation.Communications medicine · 2023Article
- Escalating Bi-Directional Feedback Loops between Proinflammatory Microglia and Mitochondria in Ageing and Post-Diagnosis of Parkinson's Disease.Antioxidants (Basel, Switzerland) · 2023Review
- Mitoferrin-1 Promotes Proliferation and Abrogates Protein Oxidation via the Glutathione Pathway in Glioblastoma.Antioxidants (Basel, Switzerland) · 2023Article
- Environmental Chemical Exposures and Mitochondrial Dysfunction: a Review of Recent Literature.Current environmental health reports · 2022Review
- Review
- Molecular and Cellular Interactions in Pathogenesis of Sporadic Parkinson Disease.International journal of molecular sciences · 2022Review
- Mitochondrial surface coating with artificial lipid membrane improves the transfer efficacy.Communications biology · 2022Article
- Metabolic Alterations in aCells · 2022Article
- Article
- Inorganic Polyphosphate, Mitochondria, and Neurodegeneration.Progress in molecular and subcellular biology · 2022Article
- Metabolic Reprogramming in HIV-Associated Neurocognitive Disorders.Frontiers in cellular neuroscience · 2022Article
- Endoplasmic Reticulum Interaction Supports Energy Production and Redox Homeostasis in Mitochondria Released from Astrocytes.Translational stroke research · 2021Article
- A High-Throughput Chemical Screen in DJ-1β Mutant Flies Identifies Zaprinast as a Potential Parkinson's Disease Treatment.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2021Article
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
Parkinson disease (PD) is a neurodegenerative disorder characterized by a selective loss of dopaminergic neurons in the substantia nigra. The earliest biochemical signs of the disease involve failure in mitochondrial-endoplasmic reticulum cross talk and lysosomal function, mitochondrial electron chain impairment, mitochondrial dynamics alterations, and calcium and iron homeostasis abnormalities. These changes are associated with increased mitochondrial reactive oxygen species (mROS) and energy deficiency. Recently, it has been reported that, as an attempt to compensate for the mitochondrial dysfunction, neurons invoke glycolysis as a low-efficient mode of energy production in models of PD. Here, we review how mitochondria orchestrate the maintenance of cellular energetic status in PD, with special focus on the switch from oxidative phosphorylation to glycolysis, as well as the implication of endoplasmic reticulum and lysosomes in the control of bioenergetics.
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.