Evidence map›Paper›PMID 23420039›Full record

ArticleJournal of molecular neuroscience : MN2013

Increased expression of Beclin-1-dependent autophagy protects against beta-amyloid-induced cell injury in PC12 cells [corrected].

Zhongfeng Xue, Sheng Zhang, Liping Huang, Yuping He, Ruoming Fang, Yongqi Fang

Erratum issuedAbstract read
PubMed Publisher
In one paragraph

Article in Journal of molecular neuroscience : MN, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
2.8field-weighted citation impact, top 9% of its field
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

15 citing papers in PubMed, 31 citations in OpenAlex.

  1. The connection between autophagy and Alzheimer's disease.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2025
    Review
  2. Review
  3. Review
  4. β-Asarone improves learning and memory in AβMetabolic brain disease · 2020
    Article
  5. Review
  6. Review
  7. Article
  8. Evaluating the Effectiveness of GTM-1, Rapamycin, and Carbamazepine on Autophagy and Alzheimer Disease.Medical science monitor : international medical journal of experimental and clinical research · 2017
    Article
  9. Article
  10. Article
  11. Article
  12. Activation of mTOR: a culprit of Alzheimer's disease?Neuropsychiatric disease and treatment · 2015
    Review
  13. Review
  14. Review
  15. Rapamycin, Autophagy, and Alzheimer's Disease.Journal of biochemical and pharmacological research · 2013
    Article
4 · The record

Corrections and comments

  • Erratum issued
5 · Who and what money

Authors and funding

6 authors at 2 institutions in 1 country.

Zhongfeng XueThe First Affiliated Hospital of Guangzhou University of Chinese Medicine, 16, Jichang Road, Guangzhou, 510405, China.
Sheng Zhang
Liping Huang
Yuping He
Ruoming Fang
Yongqi Fang
First Affiliated Hospital of Guangzhou University of Chinese Medicine · CNGuangzhou University of Chinese Medicine · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Alzheimer's disease (AD) is an age-related and progressive neurodegenerative disease. Beta-amyloid (Aβ) plays an important role in the pathogenesis of AD. Autophagy is a self-degradative process and its related protein Beclin-1 is involved in the initiation of autophagy. However, the role of Beclin-1 in the pathogenesis of AD is rarely reported. In this study, we examined cell viability and medium levels of neuron-specific enolase (NSE) in PC12 cells incubated with gradient concentrations of Aβ(1-42) (0.625, 1.25, 2.5, 5, 10 μM) for 6, 12, 24, 48, and 72 h, drew the index changes curves, and investigated the correlation between them. The result showed that cell viability was negatively correlated with NSE levels. Based on this study, Beclin-1 expression was quantitatively detected in Aβ1-42-treated PC12 cells and the dynamic changes curve of Beclin-1 was drawn from 3 to 72 h. Beclin-1 expression was positively correlated with cell viability. Furthermore, both autophagy inhibitor 3-methyladenine (3-MA) and autophagy activator rapamycin were used to investigate the effect of autophagy on Aβ(1-42)-induced cell injury. Aβ(1-42)-induced Beclin-1 expression was further upregulated by rapamycin but was downregulated by 3-MA. Moreover, cell viability was increased by rapamycin but was decreased by 3-MA, and NSE was decreased by rapamycin but was increased by 3-MA, suggesting that activation of Beclin-1-dependent autophagy before the damage occurred can prevent neuronal cell death, while inhibition of Beclin-1-dependent autophagy can hastened cell death. These findings indicate that increasing Beclin-1-dependent autophagy may have a preventive effect before the AD occurred.

Indexed as

AutophagyUp-RegulationAdenineAmyloid beta-PeptidesAnimalsApoptosis Regulatory ProteinsBeclin-1Cell DeathCell SurvivalDose-Response Relationship, DrugNeuronsPC12 CellsPeptide FragmentsPhosphopyruvate HydrataseRatsSirolimus3-methyladenineAdenineAmyloid beta-Peptidesamyloid beta-protein (1-42)Apoptosis Regulatory ProteinsBeclin-1Becn1 protein, ratPeptide FragmentsPhosphopyruvate HydrataseSirolimus

Identifiers

PMID23420039
OpenAlexW2114474227

What OpenQuestion 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 OpenQuestion graph.