Evidence map›Paper›PMID 30177770›Full record

ArticleScientific reports2018

Independent modes of disease repair by AIM protein distinguished in AIM-felinized mice.

Ryoichi Sugisawa, Ginga Komatsu, Emiri Hiramoto, Naoki Takeda, Ken-Ichi Yamamura, Satoko Arai, Toru Miyazaki

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
0.7field-weighted citation impact, top 33% 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, 15 citations in OpenAlex.

  1. Plasma Proteomic Profile of Dietary Potassium and Incident CKD.Clinical journal of the American Society of Nephrology : CJASN · 2026
    Article
  2. Article
  3. Article
  4. Review
  5. Review
  6. Article
  7. CD5L is a canonical component of circulatory IgM.Proceedings of the National Academy of Sciences of the United States of America · 2023
    Article
  8. Review
  9. Article
  10. Article
  11. Article
  12. Role of Polymeric Immunoglobulin Receptor in IgA and IgM Transcytosis.International journal of molecular sciences · 2021
    Review
  13. Review
  14. Article
  15. 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

7 authors at 4 institutions in 2 countries.

Ryoichi SugisawaLaboratory of Molecular Biomedicine for Pathogenesis, Center for Disease Biology and Integrative Medicine, Faculty of Medicine, The University of Tokyo, Tokyo, 113-0033, Japan.ORCID 0000-0002-5912-5647
Ginga KomatsuLaboratory of Molecular Biomedicine for Pathogenesis, Center for Disease Biology and Integrative Medicine, Faculty of Medicine, The University of Tokyo, Tokyo, 113-0033, Japan.
Emiri HiramotoLaboratory of Molecular Biomedicine for Pathogenesis, Center for Disease Biology and Integrative Medicine, Faculty of Medicine, The University of Tokyo, Tokyo, 113-0033, Japan.
Naoki TakedaCenter for Animal Resources and Development, Kumamoto University, Kumamoto, 860-0811, Japan.
Ken-Ichi YamamuraCenter for Animal Resources and Development, Kumamoto University, Kumamoto, 860-0811, Japan.
Satoko AraiLaboratory of Molecular Biomedicine for Pathogenesis, Center for Disease Biology and Integrative Medicine, Faculty of Medicine, The University of Tokyo, Tokyo, 113-0033, Japan.ORCID 0000-0002-6145-8686
Toru MiyazakiLaboratory of Molecular Biomedicine for Pathogenesis, Center for Disease Biology and Integrative Medicine, Faculty of Medicine, The University of Tokyo, Tokyo, 113-0033, Japan. tm@m.u-tokyo.ac.jp.
The University of Tokyo · JPKumamoto University · JPJapan Agency for Medical Research and Development · JPTrinity College Dublin · IE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Tissue macrophage-derived apoptosis inhibitor of macrophage (AIM, encoded by cd5l gene) is a circulating protein that has suppressive functions in a broad range of diseases including obesity, liver steatosis, hepatocellular carcinoma (HCC), and acute kidney injury (AKI). In healthy states, high levels of AIM circulate in the inactivated state by associating with the immunoglobulin M (IgM) pentamer in the blood, whereas during AKI, AIM dissociates from IgM and gains disease repair activity. Here, we assessed whether AIM activation via its release from IgM is required to ameliorate other diseases. To this end, we employed a mouse line in which mouse AIM was replaced with feline AIM (AIM-felinized mice). Because feline AIM rarely dissociates from IgM due to its extremely high binding affinity for IgM, these mice exhibited deficient AKI repair as in cats. When fed a high-fat diet (HFD), similar to AIM-deficient (AIM

Indexed as

AdipocytesAnimalsApoptosis Regulatory ProteinsCarcinoma, HepatocellularCatsDiet, High-FatDisease ResistanceFatty LiverGene Expression RegulationHepatocytesImmunoglobulin MKupffer CellsLiver NeoplasmsMiceMice, TransgenicObesityApoptosis Regulatory ProteinsImmunoglobulin Mpolymeric IgMReceptors, Immunologic

Identifiers

PMID30177770
PMCPMC6120884
OpenAlexW2889508720

What OpenQuestion holds

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LicenceCC BY
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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 OpenQuestion graph.