ReviewCells2019
Switching on Endogenous Metal Binding Proteins in Parkinson's Disease.
Review in Cells, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 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
21 citing papers in PubMed, 32 citations in OpenAlex.
- Crosstalk between neuroinflammation and ferroptosis: Implications for Parkinson's disease progression.Frontiers in pharmacology · 2025Review
- Metallothionein: A Comprehensive Review of Its Classification, Structure, Biological Functions, and Applications.Antioxidants (Basel, Switzerland) · 2024Review
- Dyshomeostasis of Iron and Its Transporter Proteins in Cypermethrin-Induced Parkinson's Disease.Molecular neurobiology · 2023Article
- Multifunctional Metallothioneins as a Target for Neuroprotection in Parkinson's Disease.Antioxidants (Basel, Switzerland) · 2023Review
- PCBP-1 Regulates the Transcription and Alternative Splicing of Inflammation and Ubiquitination-Related Genes in PC12 Cell.Frontiers in aging neuroscience · 2022Article
- Metals and Metal-Nanoparticles in Human Pathologies: From Exposure to Therapy.Molecules (Basel, Switzerland) · 2021Review
- Parkinson's disease: Alterations in iron and redox biology as a key to unlock therapeutic strategies.Redox biology · 2021Review
- Pathogenic mechanism and modeling of neuroferritinopathy.Cellular and molecular life sciences : CMLS · 2021Review
- Investigating the Convergent Mechanisms between Major Depressive Disorder and Parkinson's Disease.Complex psychiatry · 2021Review
- NEUROTOXICITY OF METAL MIXTURES.Advances in neurotoxicology · 2021Article
- Review
- Article
- Membrane insertion exacerbates the α-Synuclein-Cu(II) dopamine oxidase activity: Metallothionein-3 targets and silences all α-synuclein-Cu(II) complexes.Free radical biology & medicine · 2020Article
- The relationships of vitamin D, vitamin D receptor gene polymorphisms, and vitamin D supplementation with Parkinson's disease.Translational neurodegeneration · 2020Review
- Differential effects of CuBiometals : an international journal on the role of metal ions in biology, biochemistry, and medicine · 2020Article
- A Multi-Scale Computational Model of Excitotoxic Loss of Dopaminergic Cells in Parkinson's Disease.Frontiers in neuroinformatics · 2020Article
- Review
- Stem Cell Modeling of Neuroferritinopathy Reveals Iron as a Determinant of Senescence and Ferroptosis during Neuronal Aging.Stem cell reports · 2019Article
- Emerging Approaches to Investigate the Influence of Transition Metals in the Proteinopathies.Cells · 2019Article
- Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The formation of cytotoxic intracellular protein aggregates is a pathological signature of multiple neurodegenerative diseases. The principle aggregating protein in Parkinson's disease (PD) and atypical Parkinson's diseases is α-synuclein (α-syn), which occurs in neural cytoplasmic inclusions. Several factors have been found to trigger α-syn aggregation, including raised calcium, iron, and copper. Transcriptional inducers have been explored to upregulate expression of endogenous metal-binding proteins as a potential neuroprotective strategy. The vitamin-D analogue, calcipotriol, induced increased expression of the neuronal vitamin D-dependent calcium-binding protein, calbindin-D28k, and this significantly decreased the occurrence of α-syn aggregates in cells with transiently raised intracellular free Ca, thereby increasing viability. More recently, the induction of endogenous expression of the Zn and Cu binding protein, metallothionein, by the glucocorticoid analogue, dexamethasone, gave a specific reduction in Cu-dependent α-syn aggregates. Fe accumulation has long been associated with PD. Intracellularly, Fe is regulated by interactions between the Fe storage protein ferritin and Fe transporters, such as poly(C)-binding protein 1. Analysis of the transcriptional regulation of Fe binding proteins may reveal potential inducers that could modulate Fe homoeostasis in disease. The current review highlights recent studies that suggest that transcriptional inducers may have potential as novel mechanism-based drugs against metal overload in PD.
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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.