Evidence map›Paper›PMID 19656911›Full record

ArticleAmerican journal of physiology. Renal physiology2009

Uremia impacts renal inflammatory cytokine gene expression in the setting of experimental acute kidney injury.

Richard A Zager, Ali C M Johnson, Steve Lund

Open access · greenAbstract read
In one paragraph

Article in American journal of physiology. Renal physiology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed, 1 pooled it
1.8field-weighted citation impact, top 15% 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

31 citing papers in PubMed, 1 synthesis or guideline pooled it, 63 citations in OpenAlex.

  1. Pooled it
  2. A novel glomerulopathy model demonstrates renal counterbalance via local angiotensin II regulation.Proceedings of the Japan Academy. Series B, Physical and biological sciences · 2025
    Article
  3. Article
  4. Review
  5. Article
  6. Article
  7. Review
  8. Article
  9. Article
  10. Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Advances in the pathogenesis of cardiorenal syndrome type 3.Oxidative medicine and cellular longevity · 2015
    Review
  18. Article
  19. Article
  20. Review
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 2 institutions in 1 country.

Richard A ZagerFred Hutchinson Cancer Research Center, 1100 Fairview Ave. N, Rm. D2-190, Seattle, WA 98109, USA. dzager@fhcrc.org
Ali C M Johnson
Steve Lund
Fred Hutch Cancer Center · USUniversity of Washington · US

Funding

Iron Therapy in Renal Disease: Potential ToxicitiesR01DK068520 · NIDDK · FRED HUTCHINSON CANCER RESEARCH CENTER · PI ZAGER, RICHARD A. · 2004 to 2008
$1.8M
NIDDK NIH HHS R01 DK-68520PHS HHS R37 38432
6 · The paper itself

Abstract

Inflammatory cytokines are evoked by acute kidney injury (AKI) and may contribute to evolving renal disease. However, the impact of AKI-induced uremia on proinflammatory (e.g., TNF-alpha, MCP-1, TGF-beta1) and anti-inflammatory (e.g., IL-10) cytokine gene expression remains unknown. This study was undertaken to gain some initial insights into this issue. CD-1 mice were subjected to left renal ischemia-reperfusion (I/R) in the absence or presence of uremia (+/- right ureteral transection). TNF-alpha, MCP-1, TGF-beta1, and IL-10 mRNAs, cytokine protein levels, and RNA polymerase II (Pol II) recruitment to these genes were assessed. Renal cytokine mRNA levels were also contrasted with unilateral vs. bilateral renal parenchymal damage (I/R or ureteral obstruction). Potential effects of uremia on cytokine mRNAs in the absence of parenchymal renal damage [bilateral ureteral transection (BUTx)] were sought. Finally, the impact of simulated in vitro uremia (HK-2 tubular cells exposed to peritoneal dialysate from uremic vs. normal mice) on cytokine mRNA and microRNA profiles was assessed. Uremia blunted TNF-alpha, MCP-1, and TGF-beta1 mRNA increases in all three in vivo parenchymal acute renal failure models. These results were paralleled by reductions in cytokine protein levels and Pol II recruitment to their respective genes. Conversely, uremia increased IL-10 mRNA, both in the presence and absence (BUTx) of parenchymal renal damage. The uremic milieu also suppressed HK-2 cell proinflammatory cytokine mRNA levels and altered the expression of least 69 microRNAs (P < 0.0001). We conclude that both pro- and anti-inflammatory cytokine gene expressions are influenced by uremia, with a potential predilection toward an anti-inflammatory state. Changes in gene transcription (as reflected by Pol II recruitment), and possible posttranscriptional modifications (known to be induced by microRNAs), are likely involved.

Indexed as

Gene ExpressionAcute Kidney InjuryAnimalsAzotemiaCell LineChemokine CCL2ChemokinesDialysis SolutionsDNA Polymerase IIHumansInterleukin-10Kidney Tubules, ProximalLipopolysaccharidesMaleMiceMicroRNAsCcl2 protein, mouseChemokine CCL2ChemokinesDialysis SolutionsDNA Polymerase IIInterleukin-10LipopolysaccharidesMicroRNAsRNA, MessengerTransforming Growth Factor beta1Tumor Necrosis Factor-alpha

Identifiers

PMID19656911
PMCPMC2775581
OpenAlexW2126288161

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.