Evidence map›Paper›PMID 29559970›Full record

ArticleFrontiers in immunology2018

Interleukin-18 Amplifies Macrophage Polarization and Morphological Alteration, Leading to Excessive Angiogenesis.

Takuro Kobori, Shinichi Hamasaki, Atsuhiro Kitaura, Yui Yamazaki, Takashi Nishinaka, Atsuko Niwa, Shinichi Nakao, Hidenori Wake, Shuji Mori, Tadashi Yoshino and 2 more

Open access · goldAbstract read
In one paragraph

Article in Frontiers in immunology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.

0numbers the graph read from it
0cells of the map it votes in
44citing papers in PubMed
2.7field-weighted citation impact, top 10% 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

44 citing papers in PubMed, 73 citations in OpenAlex.

  1. Review
  2. Review
  3. IL18 Works Like a Two-Side Coin in Acute Pancreatitis.International journal of general medicine · 2026
    Article
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  13. Journal of agricultural and food chemistry · 2024
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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 1 country.

Takuro KoboriDepartment of Pharmacology, Faculty of Medicine, Kindai University, Osaka-Sayama, Japan.
Shinichi HamasakiDepartment of Anesthesiology, Faculty of Medicine, Kindai University, Osaka-Sayama, Japan.
Atsuhiro KitauraDepartment of Anesthesiology, Faculty of Medicine, Kindai University, Osaka-Sayama, Japan.
Yui YamazakiDepartment of Pharmacology, Faculty of Medicine, Kindai University, Osaka-Sayama, Japan.
Takashi NishinakaDepartment of Pharmacology, Faculty of Medicine, Kindai University, Osaka-Sayama, Japan.
Atsuko NiwaDepartment of Pharmacology, Faculty of Medicine, Kindai University, Osaka-Sayama, Japan.
Shinichi NakaoDepartment of Anesthesiology, Faculty of Medicine, Kindai University, Osaka-Sayama, Japan.
Hidenori WakeDepartment of Pharmacology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University, Okayama, Japan.
Shuji MoriDepartment of Pharmacology, School of Pharmacy, Shujitsu University, Okayama, Japan.
Tadashi YoshinoDepartment of Pathology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University, Okayama, Japan.
Masahiro NishiboriDepartment of Pharmacology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University, Okayama, Japan.
Hideo TakahashiDepartment of Pharmacology, Faculty of Medicine, Kindai University, Osaka-Sayama, Japan.
Kindai University · JPOkayama University · JPShujitsu University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

M2 macrophage (Mφ) promotes pathologic angiogenesis through a release of pro-angiogenic mediators or the direct cell-cell interaction with endothelium in the micromilieu of several chronic inflammatory diseases, including rheumatoid arthritis and cancer, where interleukin (IL)-18 also contributes to excessive angiogenesis. However, the detailed mechanism remains unclear. The aim of this study is to investigate the mechanism by which M2 Mφs in the micromilieu containing IL-18 induce excessive angiogenesis in the

Indexed as

AnimalsCell CommunicationCell Line, TumorCell PolarityEndothelial CellsInterleukin-10Interleukin-18MacrophagesMiceNeovascularization, PathologicOsteopontinRAW 264.7 CellsThrombinIL10 protein, mouseInterleukin-10Interleukin-18OsteopontinSpp1 protein, mouseThrombinangiogenesisCD163interleukin-18macrophageosteopontinthrombin

Identifiers

PMID29559970
PMCPMC5845536
OpenAlexW2790823487

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.