Evidence map›Paper›PMID 27623715›Full record

ArticleAging cell2017

Endogenous reactive oxygen species cause astrocyte defects and neuronal dysfunctions in the hippocampus: a new model for aging brain.

Takamasa Ishii, Yumi Takanashi, Koichi Sugita, Masaki Miyazawa, Rintaro Yanagihara, Kayo Yasuda, Hiromi Onouchi, Noboru Kawabe, Munehiro Nakata, Yorihiro Yamamoto and 2 more

Open access · goldAbstract read
In one paragraph

Article in Aging cell, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.

0numbers the graph read from it
0cells of the map it votes in
46citing papers in PubMed
3.1field-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

46 citing papers in PubMed, 72 citations in OpenAlex.

  1. Article
  2. International journal of molecular sciences · 2026
    Article
  3. Review
  4. Article
  5. Article
  6. Article
  7. Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Ageing in the brain: mechanisms and rejuvenating strategies.Cellular and molecular life sciences : CMLS · 2023
    Review
  14. Blood-CNS barrier dysfunction in amyotrophic lateral sclerosis: Proposed mechanisms and clinical implications.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2023
    Review
  15. Succinate dehydrogenase complex subunit C: Role in cellular physiology and disease.Experimental biology and medicine (Maywood, N.J.) · 2023
    Review
  16. Article
  17. Review
  18. Article
  19. Review
  20. 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

12 authors at 3 institutions in 2 countries.

Takamasa IshiiDepartment of Molecular Life Science, Tokai University School of Medicine, 143 Shimokasuya, Isehara, Kanagawa, 259-1193, Japan.
Yumi TakanashiDepartment of Molecular Life Science, Tokai University School of Medicine, 143 Shimokasuya, Isehara, Kanagawa, 259-1193, Japan.
Koichi SugitaDepartment of Molecular Life Science, Tokai University School of Medicine, 143 Shimokasuya, Isehara, Kanagawa, 259-1193, Japan.
Masaki MiyazawaDepartment of Molecular Life Science, Tokai University School of Medicine, 143 Shimokasuya, Isehara, Kanagawa, 259-1193, Japan.
Rintaro YanagiharaDepartment of Molecular Life Science, Tokai University School of Medicine, 143 Shimokasuya, Isehara, Kanagawa, 259-1193, Japan.
Kayo YasudaDepartment of Molecular Life Science, Tokai University School of Medicine, 143 Shimokasuya, Isehara, Kanagawa, 259-1193, Japan.
Hiromi OnouchiDepartment of Ophthalmology, Tokai University School of Medicine, 143 Shimokasuya, Isehara, Kanagawa, 259-1193, Japan.
Noboru KawabeSupport Center for Medical Research and Education, Tokai University, 143 Shimokasuya, Isehara, Kanagawa, 259-1193, Japan.
Munehiro NakataDepartment of Applied Biochemistry, Tokai University School of Engineering, 4-1-1 Kitakaname, Hiratsuka, Kanagawa, 259-1292, Japan.
Yorihiro YamamotoSchool of Bioscience and Biotechnology, Tokyo University of Technology, 1404-1 Katakuramachi, Hachioji, Tokyo, 192-0982, Japan.
Phil S HartmanDepartment of Biology, Texas Christian University, Fort Worth, TX, 76129, USA.
Naoaki IshiiDepartment of Molecular Life Science, Tokai University School of Medicine, 143 Shimokasuya, Isehara, Kanagawa, 259-1193, Japan.
Tokai University · JPTokyo University of Technology · JPTexas Christian University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The etiology of astrocyte dysfunction is not well understood even though neuronal defects have been extensively studied in a variety of neuronal degenerative diseases. Astrocyte defects could be triggered by the oxidative stress that occurs during physiological aging. Here, we provide evidence that intracellular or mitochondrial reactive oxygen species (ROS) at physiological levels can cause hippocampal (neuronal) dysfunctions. Specifically, we demonstrate that astrocyte defects occur in the hippocampal area of middle-aged Tet-mev-1 mice with the SDHC

Indexed as

AgingAnimalsAstrocytesBiomarkersCalciumCyclic AMP Response Element-Binding ProteinDisease Models, AnimalGlial Fibrillary Acidic ProteinHippocampusJNK Mitogen-Activated Protein KinasesMembrane ProteinsMemoryMice, Inbred C57BLMitochondriaModels, BiologicalMutationBiomarkersCalciumCyclic AMP Response Element-Binding ProteinGlial Fibrillary Acidic ProteinJNK Mitogen-Activated Protein KinasesMembrane ProteinsReactive Oxygen SpeciesS100 ProteinsSDHC protein, mouseSuperoxide DismutaseagingastrocyteCa2+JNK/SAPKmitochondriaoxidative stress

Identifiers

PMID27623715
PMCPMC5242301
OpenAlexW2520720701

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.