Evidence map›Paper›PMID 40631489›Full record

ArticleNeuroreport2025

The regulatory role of cell cycle exit and neuronal differentiation 1 in the pathogenesis of Parkinson's disease by regulating the nuclear factor kappa B pathway.

Zewei Cong, Chan Li

Abstract read
In one paragraph

Article in Neuroreport, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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0citing papers in PubMed
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1 · What the graph read from it

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2 · The registry

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3 · Its place in the literature

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4 · The record

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5 · Who and what money

Authors and funding

2 authors.

Zewei CongDepartment of Traditional Chinese Medicine, Wuhan Third Hospital, Tongren Hospital of Wuhan University, Wuhan, China.
Chan Li

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveThis study seeks to investigate the roles and underlying mechanisms of cell cycle exit and neuronal differentiation 1 (CEND1) on Parkinson's disease.

methodsReal-time quantitative PCR (RT-qPCR) was employed to assess the expression levels of CEND1 in peripheral blood samples of Parkinson's patients. A cell model of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPP + )-induced Parkinson's disease was established in-vitro. 3-[4,5-Dimethylthiazol-2-yl]-2,5 diphenyl tetrazolium bromide assays were used to evaluate the impact of CEND1 on the viability of SH-SY5Y cells induced by MPP + , while flow cytometry was used to assess apoptosis of these cells. The expression of oxidative stress and inflammatory factors in MPP + -treated cells was detected by ELISA. In addition, the effect of CEND1 on Parkinson's disease was interfered by an activator of the nuclear factor kappa B (NF-κB) pathway to clarify the relationship between CEND1 and the NF-κB pathway in a cell model of Parkinson's disease.

resultsCEND1 expression is markedly downregulated in patients with Parkinson's disease and cells of the Parkinson's disease model. Downregulation of CEND1-induced apoptosis, inhibited cell proliferation, and promoted expression of inflammatory factors in MPP + -treated cells; however, high expression of CEND1 inhibited MPP + -induced apoptosis, inflammatory factor release, and oxidative stress. In addition, CEND1 inhibited the activation of the NF-κB pathway induced by MPP + , and phorbol 12-myristate 13-acetate reversed the effect of CEND1 on Parkinson's disease.

conclusionCEND1 plays a protective role in the Parkinson's disease cell model by suppressing NF-κB signaling pathway activation, offering a potential target and foundation for the diagnosis and therapy of Parkinson's disease.

Indexed as

NF-kappa BParkinson DiseaseAgedApoptosisCell Line, TumorFemaleHumansMaleMiddle AgedOxidative StressSignal TransductionNF-kappa Bcell cycle exit and neuronal differentiationnuclear factor kappa B pathwayParkinson’s diseasephorbol 12-myristate 13-acetate

Identifiers

PMID40631489
PMCPMC13102352

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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.