Evidence map›Paper›PMID 17071582›Full record

ArticleThe American journal of pathology2006

A possible anti-inflammatory role of angiotensin II type 2 receptor in immune-mediated glomerulonephritis during type 1 receptor blockade.

Hirokazu Okada, Tsutomu Inoue, Tomohiro Kikuta, Yusuke Watanabe, Yoshihiko Kanno, Shinichi Ban, Takeshi Sugaya, Masatsugu Horiuchi, Hiromichi Suzuki

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 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.8field-weighted citation impact, top 14% 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

17 citing papers in PubMed, 41 citations in OpenAlex.

  1. Article
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  8. Review
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  12. Review
  13. LOX-1 and angiotensin receptors, and their interplay.Cardiovascular drugs and therapy · 2011
    Review
  14. Fibroblast expression of an IκB dominant-negative transgene attenuates renal fibrosis.Journal of the American Society of Nephrology : JASN · 2010
    Article
  15. Article
  16. Protective role of angiotensin II type 2 receptor signaling in a mouse model of pancreatic fibrosis.American journal of physiology. Gastrointestinal and liver physiology · 2009
    Article
  17. Poly(ADP-ribose) polymerase-1 enhances transcription of the profibrotic CCN2 gene.Journal of the American Society of Nephrology : JASN · 2008
    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

9 authors at 2 institutions in 1 country.

Hirokazu OkadaDepartment of Nephrology, Saitama Medical School, 38 Morohongo, Irumagun, Saitama 350-0495, Japan.
Tsutomu Inoue
Tomohiro Kikuta
Yusuke Watanabe
Yoshihiko Kanno
Shinichi Ban
Takeshi Sugaya
Masatsugu Horiuchi
Hiromichi Suzuki
Saitama Medical University · JPEhime University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

We previously reported that angiotensin II type 1 receptor (AT1R) blockade attenuates renal inflammation/fibrogenesis in immune-mediated glomerulonephritis via angiotensin II type 2 receptor (AT2R). In the present study, further in vivo experiments revealed that AT2R was expressed in tubular epithelial cells of nephritic kidneys in mice, and feedback activation of the renin-angiotensin system during AT1R blockade significantly reduced p-ERK, but not intranuclear nuclear factor-kappaB, levels via AT2R. This led to reduction in mRNA levels of the proinflammatory mediator monocyte chemoattractant protein-1 and overall interstitial inflammation and subsequent fibrogenesis. Specific blockade of ERK expression in tubular epithelium by anti-sense oligodeoxynucleotides also attenuated interstitial inflammation, mimicking the anti-inflammatory action of AT2R in nephritic kidneys. Alternatively, we succeeded in confirming such an AT(2)R function by demonstrating that AT1R blockade did not confer renoprotection in nephritic, AT2R gene-deficient mice. Additional in vitro experiments revealed that AT2R activation did not affect nuclear factor-kappaB activation by tumor necrosis factor-alpha in cultured tubular epithelial cells, although it inhibited ERK phosphorylation, which reduced monocyte chemoattractant protein-1 mRNA levels. These results suggest that feedback activation of AT2Rs in tubular epithelium of nephritic kidneys plays an important role in attenuating interstitial inflammation.

Indexed as

Angiotensin II Type 1 Receptor BlockersAnimalsAnti-Glomerular Basement Membrane DiseaseChemokine CCL2Enzyme ActivationEpithelial CellsEpitheliumExtracellular Signal-Regulated MAP KinasesGene Expression RegulationInflammationKidney TubulesMaleMiceNF-kappa BReceptor, Angiotensin, Type 1Receptor, Angiotensin, Type 2Angiotensin II Type 1 Receptor BlockersCcl2 protein, mouseChemokine CCL2Extracellular Signal-Regulated MAP KinasesNF-kappa BReceptor, Angiotensin, Type 1Receptor, Angiotensin, Type 2RNA, Messenger

Identifiers

PMID17071582
PMCPMC1780194
OpenAlexW1971414965

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.