Evidence mapPaperPMID 42599608Full record

ArticleNeurochemical research2026

PARK7/HSPB1-Mediated Neuroprotective Effects of SHED in an In vitro Parkinson's Disease Model.

Yiqi Yu, Hongyu Chen, Jinglei Zheng, Shuting Liu, Xiao Wang, Cencan Xing, Hongwu Du

Abstract read
PubMed Publisher
In one paragraph

Article in Neurochemical research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
field-weighted citation impact
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

7 authors.

Yiqi Yu *School of Chemistry and Biological Engineering, University of Science and Technology Beijing, Beijing, 100083, China.
Hongyu Chen *School of Chemistry and Biological Engineering, University of Science and Technology Beijing, Beijing, 100083, China.
Jinglei Zheng *Department of Stomatology, Peking University Third Hospital, Beijing, 100191, China.
Shuting LiuSchool of Chemistry and Biological Engineering, University of Science and Technology Beijing, Beijing, 100083, China.
Xiao WangDepartment of Stomatology, Peking University Third Hospital, Beijing, 100191, China. 9363170498@bjmu.edu.cn.
Cencan XingSchool of Chemistry and Biological Engineering, University of Science and Technology Beijing, Beijing, 100083, China. cencanxing@ustb.edu.cn.
Hongwu DuSchool of Chemistry and Biological Engineering, University of Science and Technology Beijing, Beijing, 100083, China. hongwudu@ustb.edu.cn.

Funding

Beijing Science & Technology New Star Cross Project 20240484705National Natural Science Foundation of China 32300682the Interdisciplinary Research Project for Young Teachers of USTB FRF-IDRY-21-031
6 · The paper itself

Abstract

Parkinson's disease (PD) is a neurodegenerative disease characterized by progressive loss of dopaminergic neurons. Studies have shown that mesenchymal stem cells (MSCs) have prominent neuroprotective potential to improve PD. Previous study found that dental pulp‑derived MSCs, including stem cells from human exfoliated deciduous teeth (SHED), significantly ameliorated PD-related pathology, but the underlying molecular mechanism remains unclear. In this study, HSPB1 and PARK7 were initially identified through transcriptomic analyses of mouse and clinical samples, immunoprecipitation‑mass spectrometry (IP‑pulldown), and protein‑protein interaction (PPI) network analysis. Using an MPTP-induced SH-SY5Y cell model of PD, we found that SHED treatment alleviated oxidative stress, restored mitochondrial membrane potential, and inhibited apoptosis, accompanied by significant upregulation of HSPB1 and PARK7. Using siRNA interference, we confirmed that both HSPB1 and PARK7 are involved in the improvement of PD by SHED. Rescue experiments showed that HSPB1 overexpression partially restored the neuroprotective effects impaired by PARK7 knockdown, whereas PARK7 overexpression failed to compensate for HSPB1 deficiency, suggesting a functional dependence between PARK7 and HSPB1 in SHED-mediated neuroprotection. This study demonstrates that SHED improves PD pathological progression through the PARK7/HSPB1-related mechanism and indicates that HSPB1 may serve as a potential therapeutic target for PD.

Indexed as

Heat-Shock ProteinsHSP27 Heat-Shock ProteinsMesenchymal Stem CellsMolecular ChaperonesParkinson DiseaseProtein Deglycase DJ-1AnimalsApoptosisCell Line, TumorHumansMaleMembrane Potential, MitochondrialMiceMice, Inbred C57BLOxidative StressHeat-Shock ProteinsHsbp1 protein, mouseHSP27 Heat-Shock ProteinsHSPB1 protein, humanMolecular ChaperonesPARK7 protein, humanPARK7 protein, mouseProtein Deglycase DJ-1HSPB1PARK7Parkinson’s diseaseStem cells

Identifiers

What Socratic holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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 Socratic graph.