Evidence map›Paper›PMID 33002038›Full record

ArticlePloS one2020

Thermal cycling protects SH-SY5Y cells against hydrogen peroxide and β-amyloid-induced cell injury through stress response mechanisms involving Akt pathway.

Wei-Ting Chen, Yu-Yi Kuo, Guan-Bo Lin, Chueh-Hsuan Lu, Hao-Ping Hsu, Yi-Kun Sun, Chih-Yu Chao

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
0.8field-weighted citation impact, top 27% 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

6 citing papers in PubMed, 16 citations in OpenAlex.

  1. Article
  2. Thermal Cycling Stimulation via Nasal Inhalation Attenuates AβInternational journal of molecular sciences · 2025
    Article
  3. Article
  4. VANL-100 Attenuates Beta-Amyloid-Induced Toxicity in SH-SY5Y Cells.International journal of molecular sciences · 2022
    Article
  5. Article
  6. Review
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 at 1 institution in 1 country.

Wei-Ting ChenDepartment of Physics, Lab for Medical Physics & Biomedical Engineering, National Taiwan University, Taipei, Taiwan.
Yu-Yi KuoDepartment of Physics, Lab for Medical Physics & Biomedical Engineering, National Taiwan University, Taipei, Taiwan.
Guan-Bo LinDepartment of Physics, Lab for Medical Physics & Biomedical Engineering, National Taiwan University, Taipei, Taiwan.
Chueh-Hsuan LuDepartment of Physics, Lab for Medical Physics & Biomedical Engineering, National Taiwan University, Taipei, Taiwan.
Hao-Ping HsuDepartment of Medicine, National Taiwan University College of Medicine, Taipei, Taiwan.
Yi-Kun SunBiomedical & Molecular Imaging Center, National Taiwan University College of Medicine, Taipei, Taiwan.
Chih-Yu ChaoDepartment of Physics, Lab for Medical Physics & Biomedical Engineering, National Taiwan University, Taipei, Taiwan.ORCID 0000-0002-9792-7034
National Taiwan University · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Neurodegenerative diseases (NDDs) are becoming a major threat to public health, according to the World Health Organization (WHO). The most common form of NDDs is Alzheimer's disease (AD), boasting 60-70% share. Although some debates still exist, excessive aggregation of β-amyloid protein (Aβ) and neurofibrillary tangles has been deemed one of the major causes for the pathogenesis of AD. A growing number of evidences from studies, however, have suggested that reactive oxygen species (ROS) also play a key role in the onset and progression of AD. Although scientists have had some understanding of the pathogenesis of AD, the disease still cannot be cured, with existing treatment only capable of providing a temporary relief at best, partly due to the obstacle of blood-brain barrier (BBB). The study was aimed to ascertain the neuroprotective effect of thermal cycle hyperthermia (TC-HT) against hydrogen peroxide (H2O2) and Aβ-induced cytotoxicity in SH-SY5Y cells. Treating cells with this physical stimulation beforehand significantly improved the cell viability and decreased the ROS content. The underlying mechanisms may be due to the activation of Akt pathway and the downstream antioxidant and prosurvival proteins. The findings manifest significant potential of TC-HT in neuroprotection, via inhibition of oxidative stress and cell apoptosis. It is believed that coupled with the use of drugs or natural compounds, this methodology can be even more effective in treating NDDs.

Indexed as

Hyperthermia, InducedAmyloid beta-PeptidesCell Line, TumorCyclic AMP Response Element-Binding ProteinGene Expression RegulationHeat-Shock ProteinsHumansHydrogen PeroxideInsulysinMatrix MetalloproteinasesNF-E2-Related Factor 2Oxidative StressProteasome Endopeptidase ComplexProto-Oncogene Proteins c-aktSignal TransductionAmyloid beta-PeptidesCyclic AMP Response Element-Binding ProteinHeat-Shock ProteinsHydrogen PeroxideInsulysinMatrix MetalloproteinasesNFE2L2 protein, humanNF-E2-Related Factor 2Proteasome Endopeptidase ComplexProto-Oncogene Proteins c-akt

Identifiers

PMID33002038
PMCPMC7529293
OpenAlexW3090889172

What OpenQuestion holds

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LicenceCC BY
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.