Evidence map›Paper›PMID 40495165›Full record

ArticleMolecular medicine (Cambridge, Mass.)2025

VILIP3 attenuates neuronal apoptosis and oxidative stress via Nrf2 activation in the pathogenesis of Alzheimer's disease.

Shasha Huangfu, Xiaoyu Sang, Shiyue Zhou, Haixia Liu, Dongqing Cui, Yansheng Du, Xinyue Xing, Wenyan Liu, Jianzhong Bi, Zhaohong Xie

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In one paragraph

Article in Molecular medicine (Cambridge, Mass.), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

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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

1 citing paper in PubMed.

  1. Article
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

10 authors.

Shasha HuangfuDepartment of Neurology, The Second Hospital, Cheeloo College of Medicine, Shandong University, Jinan, 250033, China.
Xiaoyu SangDepartment of Neurology, The Second Hospital, Cheeloo College of Medicine, Shandong University, Jinan, 250033, China.
Shiyue ZhouDepartment of Neurology, The Second Hospital, Cheeloo College of Medicine, Shandong University, Jinan, 250033, China.
Haixia LiuDepartment of Neurology, The Second Hospital, Cheeloo College of Medicine, Shandong University, Jinan, 250033, China.
Dongqing CuiDepartment of Neurology, The Second Hospital, Cheeloo College of Medicine, Shandong University, Jinan, 250033, China.
Yansheng DuDepartment of Neurology, The Second Hospital, Cheeloo College of Medicine, Shandong University, Jinan, 250033, China.
Xinyue XingDepartment of Neurology, The Second Hospital, Cheeloo College of Medicine, Shandong University, Jinan, 250033, China.
Wenyan LiuDepartment of Neurology, The Second Hospital, Cheeloo College of Medicine, Shandong University, Jinan, 250033, China.
Jianzhong BiDepartment of Neurology, The Second Hospital, Cheeloo College of Medicine, Shandong University, Jinan, 250033, China.
Zhaohong XieDepartment of Neurology, The Second Hospital, Cheeloo College of Medicine, Shandong University, Jinan, 250033, China. xie_zhaohong@sdu.edu.cn.

Funding

Shandong University Multidisciplinary Research and Innovation Team of Young Scholars 2020QNQT019The National Natural Science Foundation of China 81870848
6 · The paper itself

Abstract

backgroundAlzheimer’s disease (AD) is a common neurodegenerative condition characterized by amyloid-β protein (Aβ) deposition, which is central to its pathological changes. Oxidative stress also plays an important role in its pathogenesis. Visinin-like protein 3 (VILIP3), a neuronal calcium sensor protein, is abnormally expressed in the brains of patients with AD; however, the exact mechanism remains unclear. This study investigated the role of abnormal VILIP3 expression in AD pathogenesis and its underlying mechanisms.

methodsWe used 5×FAD mice as an in vivo model of AD and Aβ1−42-treated SH-SY5Y cells to construct an in vitro model. Changes in VILIP3 expression were assessed in both models. VILIP3 was overexpressed in the hippocampus of 5×FAD mice and SH-SY5Y cells using adeno-associated virus (AAV) or plasmid transfection. Cognitive function, Aβ deposition, neuronal damage, synaptic plasticity, apoptosis, oxidative stress, and other relevant indices were evaluated.

resultsVILIP3 was expressed at lower levels in AD model mice and cells than in controls. Overexpression of VILIP3 ameliorated cognitive deficits, reduced Aβ deposition and neuronal loss in 5×FAD mice, and attenuated oxidative stress levels and apoptosis in 5×FAD mice and Aβ1−42-treated SH-SY5Y cells. Furthermore, VILIP3 activated nuclear factor E2-related factor 2 (Nrf2) and increased the expression of downstream antioxidant genes. The amelioration of apoptosis and oxidative stress by VILIP3 was blocked by Nrf2-specific inhibitors.

conclusionsVILIP3 mitigates oxidative stress and apoptosis by activating the Nrf2 signaling pathway, thereby alleviating neuropathological damage and cognitive dysfunction in AD.

Indexed as

Alzheimer DiseaseApoptosisNeurocalcinNeuronsNF-E2-Related Factor 2Oxidative StressAmyloid beta-PeptidesAnimalsCell Line, TumorDisease Models, AnimalHippocampusHumansMaleMiceMice, TransgenicSignal TransductionAmyloid beta-PeptidesNeurocalcinNF-E2-Related Factor 2Alzheimer’s diseaseApoptosisNeuroprotectionNrf2Oxidative stressVILIP3

Identifiers

PMID40495165
PMCPMC12150439

What Socratic holds

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Registered trials

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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 Socratic graph.