Evidence map›Paper›PMID 21821915›Full record

ArticleThe Journal of clinical investigation2011

Renal collecting duct epithelial cells regulate inflammation in tubulointerstitial damage in mice.

Katsuhito Fujiu, Ichiro Manabe, Ryozo Nagai

Open access · greenAbstract read
In one paragraph

Article in The Journal of clinical investigation, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 125 papers.

0numbers the graph read from it
0cells of the map it votes in
125citing papers in PubMed
8.0field-weighted citation impact, top 2% 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

125 citing papers in PubMed, 246 citations in OpenAlex.

  1. Trial
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  7. Integrins in the kidney - beyond the matrix.Nature reviews. Nephrology · 2025
    Review
  8. Article
  9. Review
  10. Article
  11. Article
  12. Article
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  14. Activation of the YAP/KLF5 transcriptional cascade in renal tubular cells aggravates kidney injury.Molecular therapy : the journal of the American Society of Gene Therapy · 2024
    Article
  15. Article
  16. Plasma NGAL levels in stable kidney transplant recipients and the risk of allograft loss.Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association · 2024
    Article
  17. Review
  18. Resolvin D1 (Rvd1) AttenuatesReports of biochemistry & molecular biology · 2024
    Article
  19. Review
  20. Article

65 more citing papers are in PubMed but not listed here.

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

3 authors at 1 institution in 1 country.

Katsuhito FujiuDepartment of Cardiovascular Medicine, University of Tokyo Graduate School of Medicine, Bunkyo, Tokyo, Japan.
Ichiro Manabe
Ryozo Nagai
Botswana-Baylor Children's Clinical Center of Excellence · BW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Renal tubulointerstitial damage is the final common pathway leading from chronic kidney disease to end-stage renal disease. Inflammation is clearly involved in tubulointerstitial injury, but it remains unclear how the inflammatory processes are initiated and regulated. Here, we have shown that in the mouse kidney, the transcription factor Krüppel-like factor-5 (KLF5) is mainly expressed in collecting duct epithelial cells and that Klf5 haploinsufficient mice (Klf5+/- mice) exhibit ameliorated renal injury in the unilateral ureteral obstruction (UUO) model of tubulointerstitial disease. Additionally, Klf5 haploinsufficiency reduced accumulation of CD11b+ F4/80(lo) cells, which expressed proinflammatory cytokines and induced apoptosis among renal epithelial cells, phenotypes indicative of M1-type macrophages. By contrast, it increased accumulation of CD11b+ F4/80(hi) macrophages, which expressed CD206 and CD301 and contributed to fibrosis, in part via TGF-β production--phenotypes indicative of M2-type macrophages. Interestingly, KLF5, in concert with C/EBPα, was found to induce expression of the chemotactic proteins S100A8 and S100A9, which recruited inflammatory monocytes to the kidneys and promoted their activation into M1-type macrophages. Finally, assessing the effects of bone marrow-specific Klf5 haploinsufficiency or collecting duct- or myeloid cell-specific Klf5 deletion confirmed that collecting duct expression of Klf5 is essential for inflammatory responses to UUO. Taken together, our results demonstrate that the renal collecting duct plays a pivotal role in the initiation and progression of tubulointerstitial inflammation.

Indexed as

AnimalsCalgranulin ACalgranulin BCCAAT-Enhancer-Binding ProteinsCell LineCytokinesEpithelial CellsInflammationKidney Failure, ChronicKidney Tubules, CollectingKruppel-Like Transcription FactorsMacrophagesMiceNephritis, InterstitialCalgranulin ACalgranulin BCCAAT-Enhancer-Binding ProteinsCEBPA protein, mouseCytokinesKlf5 protein, mouseKruppel-Like Transcription FactorsS100a8 protein, mouse

Identifiers

PMID21821915
PMCPMC3163964
OpenAlexW2031515819

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.