ArticleMolecular neurobiology2025
Deletion of ZNRF2 Exacerbates MPTP-Induced Parkinson's Disease by Activating mTOR-Mediated Neuroinflammatory Pathways.
Article in Molecular neurobiology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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
1 citing paper in PubMed.
- Zinc finger proteins (ZFPs) in health and disease.Molecular biomedicine · 2026Review
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.
Funding
Abstract
Parkinson's disease (PD) imposes a significant health burden among older adults and may be related to zinc and ring finger 2 (ZNRF2)-a member of the ubiquitination family. To investigate the role and mechanism of action of ZNRF2 in the regulation of mammalian target of rapamycin (mTOR)-mediated neuroinflammation in a mouse model of PD. Healthy mice were injected intraperitoneally with either saline (control) or MPTP 30 mg/kg. Mouse behavior was tested using rotarod and open field tests. The distribution and expression of tyrosine hydroxylase (TH) were determined by immunoblotting and immunohistochemistry. Inflammatory factors were evaluated using immunoblotting, enzyme-linked immunosorbent assay, and immunofluorescence assay. Compared with mice injected with saline, MPTP-treated mice showed significantly impaired locomotor activity, a significant decrease in the number of TH neurons, and a markedly altered morphology. ZNRF2 expression was significantly increased in the mesencephalon of MPTP-treated mice compared to that in control mice. ZNRF2 knockdown exacerbated motor dysfunction, accelerated dopamine neuron degeneration and death, increased the levels of pro-inflammatory factors (e.g., interleukin (IL)-1β, IL-6), and suppressed the expression of anti-inflammatory factors (e.g., IL-4, IL-10) in the central nervous system of MPTP-treated mice, with more pronounced activation of microglia and astrocytes. ZNRF2 knockdown significantly elevated phosphorylated mTOR protein levels after MPTP treatment; subsequently, phosphorylated mTOR protein levels were inhibited; dyskinesia and dopamine neuronal damage were significantly ameliorated, and neuroinflammation was suppressed in PD mice. ZNRF2 regulates the pathogenesis of MPTP-induced PD in mice via mechanisms related to mTOR-mediated neuroinflammation.
Indexed as
Identifiers
40402410What 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.