Evidence map›Paper›PMID 22357963›Full record

ArticleDiabetes2012

Cholecystokinin plays a novel protective role in diabetic kidney through anti-inflammatory actions on macrophage: anti-inflammatory effect of cholecystokinin.

Satoshi Miyamoto, Kenichi Shikata, Kyoko Miyasaka, Shinichi Okada, Motofumi Sasaki, Ryo Kodera, Daisho Hirota, Nobuo Kajitani, Tetsuharu Takatsuka, Hitomi Usui Kataoka and 7 more

Open access · hybridAbstract read
In one paragraph

Article in Diabetes, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed
2.6field-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

42 citing papers in PubMed, 72 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Targeting Macrophages: Therapeutic Approaches in Diabetic Kidney Disease.International journal of molecular sciences · 2024
    Review
  5. Article
  6. Article
  7. Review
  8. Article
  9. Cholecystokinin attenuates β-cell apoptosis in both mouse and human islets.Translational research : the journal of laboratory and clinical medicine · 2022
    Article
  10. Review
  11. Review
  12. Review
  13. Article
  14. Review
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Cholecystokinin, gastrin, cholecystokinin/gastrin receptors, and bitter taste receptor TAS2R14: trophoblast expression and signaling.American journal of physiology. Regulatory, integrative and comparative physiology · 2019
    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

17 authors at 3 institutions in 1 country.

Satoshi MiyamotoDepartment of Medicine and Clinical Science, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama, Japan. shikata@md.okayama-u.ac.jp
Kenichi Shikata
Kyoko Miyasaka
Shinichi Okada
Motofumi Sasaki
Ryo Kodera
Daisho Hirota
Nobuo Kajitani
Tetsuharu Takatsuka
Hitomi Usui Kataoka
Shingo Nishishita
Chikage Sato
Akihiro Funakoshi
Hisakazu Nishimori
Haruhito Adam Uchida
Daisuke Ogawa
Hirofumi Makino
Okayama University · JPNational Hospital Organization Kyushu Cancer Center · JPTokyo Kasei University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Inflammatory process is involved in the pathogenesis of diabetic nephropathy. In this article, we show that cholecystokinin (CCK) is expressed in the kidney and exerts renoprotective effects through its anti-inflammatory actions. DNA microarray showed that CCK was upregulated in the kidney of diabetic wild-type (WT) mice but not in diabetic intracellular adhesion molecule-1 knockout mice. We induced diabetes in CCK-1 receptor (CCK-1R) and CCK-2R double-knockout (CCK-1R(-/-),-2R(-/-)) mice, and furthermore, we performed a bone marrow transplantation study using CCK-1R(-/-) mice to determine the role of CCK-1R on macrophages in the diabetic kidney. Diabetic CCK-1R(-/-),-2R(-/-) mice revealed enhanced albuminuria and inflammation in the kidney compared with diabetic WT mice. In addition, diabetic WT mice with CCK-1R(-/-) bone marrow-derived cells developed more albuminuria than diabetic CCK-1R(-/-) mice with WT bone marrow-derived cells. Administration of sulfated cholecystokinin octapeptide (CCK-8S) ameliorated albuminuria, podocyte loss, expression of proinflammatory genes, and infiltration of macrophages in the kidneys of diabetic rats. Furthermore, CCK-8S inhibited both expression of tumor necrosis factor-α and chemotaxis in cultured THP-1 cells. These results suggest that CCK suppresses the activation of macrophage and expression of proinflammatory genes in diabetic kidney. Our findings may provide a novel strategy of therapy for the early stage of diabetic nephropathy.

Indexed as

AnimalsChemokines, CCChemotaxisCholecystokininDiabetes MellitusGene Expression ProfilingGene Expression RegulationInflammationIntercellular Adhesion Molecule-1KidneyMacrophagesMaleMiceMice, KnockoutNF-kappa BReceptor, Cholecystokinin B8-sulfocholecystokinin octapeptideCcl28 protein, mouseChemokines, CCCholecystokininIntercellular Adhesion Molecule-1NF-kappa BReceptor, Cholecystokinin BReceptors, CholecystokininSincalideTumor Necrosis Factor-alpha

Identifiers

PMID22357963
PMCPMC3314350
OpenAlexW2113355485

What OpenQuestion holds

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LicenceCC BY-NC-ND
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.