Evidence map›Paper›PMID 35457223›Full record

ArticleInternational journal of molecular sciences2022

Docosahexaenoic Acid Suppresses Oxidative Stress-Induced Autophagy and Cell Death via the AMPK-Dependent Signaling Pathway in Immortalized Fischer Rat Schwann Cells 1.

Yasuaki Tatsumi, Ayako Kato, Naoko Niimi, Hideji Yako, Tatsuhito Himeno, Masaki Kondo, Shin Tsunekawa, Yoshiro Kato, Hideki Kamiya, Jiro Nakamura and 3 more

Open access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
2.3field-weighted citation impact, top 11% 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

12 citing papers in PubMed, 15 citations in OpenAlex.

  1. Article
  2. Review
  3. Broadband Collision-Induced Dissociation Mass Spectrometry Imaging.Journal of the American Society for Mass Spectrometry · 2025
    Article
  4. Review
  5. Article
  6. Article
  7. Review
  8. Unlocking the potential ofFrontiers in microbiology · 2024
    Article
  9. Review
  10. Review
  11. Article
  12. 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

13 authors at 4 institutions in 1 country.

Yasuaki TatsumiLaboratory of Medicine, Aichi Gakuin University School of Pharmacy, 1-100 Kusumoto-cho, Chikusa-ku, Nagoya 464-8650, Japan.ORCID 0000-0001-5202-7027
Ayako KatoLaboratory of Medicine, Aichi Gakuin University School of Pharmacy, 1-100 Kusumoto-cho, Chikusa-ku, Nagoya 464-8650, Japan.
Naoko NiimiDiabetic Neuropathy Project, Department of Diseases and Infection, Tokyo Metropolitan Institute of Medical Science, 2-1-6 Kamikitazawa, Setagaya, Tokyo 156-8506, Japan.
Hideji YakoDiabetic Neuropathy Project, Department of Diseases and Infection, Tokyo Metropolitan Institute of Medical Science, 2-1-6 Kamikitazawa, Setagaya, Tokyo 156-8506, Japan.ORCID 0000-0003-2632-8488
Tatsuhito HimenoDivision of Diabetes, Department of Internal Medicine, Aichi Medical University School of Medicine, 1-1 Yazakokarimate, Nagakute 480-1195, Japan.
Masaki KondoDivision of Diabetes, Department of Internal Medicine, Aichi Medical University School of Medicine, 1-1 Yazakokarimate, Nagakute 480-1195, Japan.
Shin TsunekawaDivision of Diabetes, Department of Internal Medicine, Aichi Medical University School of Medicine, 1-1 Yazakokarimate, Nagakute 480-1195, Japan.ORCID 0000-0002-9890-5777
Yoshiro KatoDivision of Diabetes, Department of Internal Medicine, Aichi Medical University School of Medicine, 1-1 Yazakokarimate, Nagakute 480-1195, Japan.
Hideki KamiyaDivision of Diabetes, Department of Internal Medicine, Aichi Medical University School of Medicine, 1-1 Yazakokarimate, Nagakute 480-1195, Japan.
Jiro NakamuraDivision of Diabetes, Department of Internal Medicine, Aichi Medical University School of Medicine, 1-1 Yazakokarimate, Nagakute 480-1195, Japan.
Koji HigaiDepartment of Medical Biochemistry, Faculty of Pharmaceutical Sciences, Toho University, Miyama 2-2-1, Funabashi 274-8510, Japan.
Kazunori SangoDiabetic Neuropathy Project, Department of Diseases and Infection, Tokyo Metropolitan Institute of Medical Science, 2-1-6 Kamikitazawa, Setagaya, Tokyo 156-8506, Japan.ORCID 0000-0002-9750-9596
Koichi KatoLaboratory of Medicine, Aichi Gakuin University School of Pharmacy, 1-100 Kusumoto-cho, Chikusa-ku, Nagoya 464-8650, Japan.
Aichi Medical University · JPTokyo Metropolitan Institute of Medical Science · JPAichi Gakuin University · JPToho University · JP

Funding

JSPS KAKENHI 18K06763
6 · The paper itself

Abstract

Autophagy is the process by which intracellular components are degraded by lysosomes. It is also activated by oxidative stress; hence, autophagy is thought to be closely related to oxidative stress, one of the major causes of diabetic neuropathy. We previously reported that docosahexaenoic acid (DHA) and eicosapentaenoic acid (EPA) induced antioxidant enzymes and protected Schwann cells from oxidative stress. However, the relationship between autophagy and oxidative stress-induced cell death in diabetic neuropathy has not been elucidated. Treatment with tert-butyl hydroperoxide (tBHP) decreased the cell survival rate, as measured by an MTT assay in immortalized Fischer rat Schwann cells 1 (IFRS1). A DHA pretreatment significantly prevented tBHP-induced cytotoxicity. tBHP increased autophagy, which was revealed by the ratio of the initiation markers, AMP-activated protein kinase, and UNC51-like kinase phosphorylation. Conversely, the DHA pretreatment suppressed excessive tBHP-induced autophagy signaling. Autophagosomes induced by tBHP in IFRS1 cells were decreased to control levels by the DHA pretreatment whereas autolysosomes were only partially decreased. These results suggest that DHA attenuated excessive autophagy induced by oxidative stress in Schwann cells and may be useful to prevent or reduce cell death in vitro. However, its potentiality to treat diabetic neuropathy must be validated in in vivo studies.

Indexed as

Diabetic NeuropathiesDocosahexaenoic AcidsAMP-Activated Protein KinasesAnimalsAutophagyCell DeathOxidative StressRatsRats, Inbred F344Schwann CellsSignal Transductiontert-ButylhydroperoxideAMP-Activated Protein KinasesDocosahexaenoic Acidstert-ButylhydroperoxideAMPKautophagyDHAoxidative stressSchwann cells

Identifiers

PMID35457223
PMCPMC9027959
OpenAlexW4224132030

What OpenQuestion holds

Textmetadata
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.