Evidence map›Paper›PMID 16651609›Full record

ArticleThe American journal of pathology2006

Attenuation of folic acid-induced renal inflammatory injury in platelet-activating factor receptor-deficient mice.

Kent Doi, Koji Okamoto, Kousuke Negishi, Yoshifumi Suzuki, Akihide Nakao, Toshiro Fujita, Akiko Toda, Takehiko Yokomizo, Yoshihiro Kita, Yasuyuki Kihara and 3 more

Open access · bronzeAbstract read
In one paragraph

Article in The American journal of pathology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed, 1 pooled it
2.3field-weighted citation impact, top 12% 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

36 citing papers in PubMed, 1 synthesis or guideline pooled it, 77 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Article
  5. Article
  6. Folic acid-induced animal model of kidney disease.Animal models and experimental medicine · 2021
    Review
  7. Article
  8. Article
  9. Review
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  14. Article
  15. Review
  16. Sphingosine Kinase 2 Deficiency Attenuates Kidney FibrosisJournal of the American Society of Nephrology : JASN · 2017
    Article
  17. Mitogen-Activated Protein Kinase 14 Promotes AKI.Journal of the American Society of Nephrology : JASN · 2017
    Article
  18. Article
  19. Article
  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

13 authors at 2 institutions in 1 country.

Kent DoiDepartment of Nephrology and Endocrinology, University of Tokyo, 7-3-1 Hongo, Bunkyo, Tokyo 113-8655, Japan.
Koji Okamoto
Kousuke Negishi
Yoshifumi Suzuki
Akihide Nakao
Toshiro Fujita
Akiko Toda
Takehiko Yokomizo
Yoshihiro Kita
Yasuyuki Kihara
Satoshi Ishii
Takao Shimizu
Eisei Noiri
The University of Tokyo · JPTokyo City University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Platelet-activating factor (PAF), a potent lipid mediator with various biological activities, plays an important role in inflammation by recruiting leukocytes. In this study we used platelet-activating factor receptor (PAFR)-deficient mice to elucidate the role of PAF in inflammatory renal injury induced by folic acid administration. PAFR-deficient mice showed significant amelioration of renal dysfunction and pathological findings such as acute tubular damage with neutrophil infiltration, lipid peroxidation observed with antibody to 4-hydroxy-2-hexenal (day 2), and interstitial fibrosis with macrophage infiltration associated with expression of monocyte chemoattractant protein-1 and tumor necrosis factor-alpha in the kidney (day 14). Acute tubular damage was attenuated by neutrophil depletion using a monoclonal antibody (RB6-8C5), demonstrating the contribution of neutrophils to acute phase injury. Macrophage infiltration was also decreased when treatment with a PAF antagonist (WEB2086) was started after acute phase. In vitro chemotaxis assay using a Boyden chamber demonstrated that PAF exhibits a strong chemotactic activity for macrophages. These results indicate that PAF is involved in pathogenesis of folic acid-induced renal injury by activating neutrophils in acute phase and macrophages in chronic interstitial fibrosis. Inhibiting the PAF pathway might be therapeutic to kidney injury from inflammatory cells.

Indexed as

Folic AcidAnimalsChemokine CCL2ChemotaxisFibrosisInflammationKidney DiseasesLeukocytesMacrophagesMiceMice, Inbred C57BLMice, KnockoutMice, TransgenicNeutrophilsPlatelet Activating FactorPlatelet Membrane GlycoproteinsCcl2 protein, mouseChemokine CCL2Folic AcidPlatelet Activating Factorplatelet activating factor receptorPlatelet Membrane GlycoproteinsReactive Oxygen SpeciesReceptors, G-Protein-CoupledTumor Necrosis Factor-alpha

Identifiers

PMID16651609
PMCPMC1606605
OpenAlexW2029746669

What OpenQuestion holds

Textmetadata
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.