ArticleMolecular neurobiology2026
VSIG4 Inhibits Microglia-Mediated Neuroinflammation and Neuronal Injury by Modulating the JAK2-STAT3/NF-κB Signaling Pathway in Parkinson's Disease.
Article in Molecular neurobiology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
V-set and immunoglobulin domain-containing 4 (VSIG4) was found to regulate microglial inflammation and oxidative stress in our previous study. This study aimed to further explore the effect and mechanism of VSIG4 on neuroinflammation and neuronal injury in Parkinson's disease (PD). Mouse microglia were infected with VSIG4-overexpressing adeno-associated virus (AAV) or shRNA AAV or VSIG4-overexpressing AAV with or without AZD1480 (a JAK inhibitor). Furthermore, a coculture system was established, where mouse dopamine neurons were cocultured with the infected microglia or their culture medium under the presence of α-synuclein. PD mice were treated with VSIG4-overexpressing AAV, with or without AZD1480. In microglia, VSIG4 overexpression inhibited the release of tumor necrosis factor-α, interleukin-6, and interleukin-1β and modulated the JAK2-STAT3/NF-κB pathway, but its knockdown had the opposite effect. In the coculture system, VSIG4-overexpressing microglia promoted dopamine neuron viability but suppressed p-α-synuclein and neuron apoptosis, whereas VSIG4-knockdown microglia presented the opposite effect. The culture medium of VSIG4-modified microglia had a similar effect on dopamine neuron functions to that of VSIG4-modified microglia. In PD mice, VSIG4 was insufficiently expressed in microglia, while VSIG4 overexpression improved the performances in open field and pole tests, promoted dopamine neuron viability and dopamine transport, and suppressed p-α-synuclein and neuroinflammation. Moreover, the addition of AZD1480 attenuated the effects of VSIG4 overexpression both in vitro and in vivo. VSIG4 ameliorates microglia-mediated neuroinflammation and neuronal injury via the JAK2-STAT3/NF-κB pathway in PD, shedding light on its supplementation as a potential treatment option for PD.
Indexed as
Identifiers
42661115What 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.