Evidence map›Paper›PMID 23234871›Full record

ArticleNephron. Experimental nephrology2012

Podocytes express IL-6 and lipocalin 2/ neutrophil gelatinase-associated lipocalin in lipopolysaccharide-induced acute glomerular injury.

Sarah J Lee, Emily Borsting, Anne-Emilie Declèves, Prabhleen Singh, Robyn Cunard

Open access · bronzeAbstract read
In one paragraph

Article in Nephron. Experimental nephrology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
2.2field-weighted citation impact, top 13% 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

19 citing papers in PubMed, 35 citations in OpenAlex.

  1. Inflammation in glomerular diseases.Frontiers in immunology · 2025
    Review
  2. IL-6 and diabetic kidney disease.Frontiers in immunology · 2024
    Review
  3. Review
  4. Parthenolide Attenuates Sepsis-Induced Acute Kidney Injury in Rats by Reducing Inflammation.Evidence-based complementary and alternative medicine : eCAM · 2023
    Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Review
  12. IL-33/ST2 Axis in Organ Fibrosis.Frontiers in immunology · 2018
    Review
  13. Review
  14. Article
  15. Article
  16. IL-6 Trans-Signaling Drives Murine Crescentic GN.Journal of the American Society of Nephrology : JASN · 2016
    Article
  17. Review
  18. Article
  19. 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

5 authors at 2 institutions in 1 country.

Sarah J LeeResearch Service and Division of Nephrology-Hypertension, Veterans Affairs San Diego Healthcare System, Veterans Medical Research Foundation, San Diego, CA 92161, USA.
Emily Borsting
Anne-Emilie Declèves
Prabhleen Singh
Robyn Cunard
University of California, San Diego · USVeterans Medical Research Foundation of San Diego · US

Funding

Transgenic & Knock-out MouseP30DK063491 · NIDDK · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI MILES Frome WILKINSON · 2003 to 2026
$40.4M
Pathophysiology of Early Chronic Kidney Disease: Response to Ischemia-ReperfusionK08DK084305 · NIDDK · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI SINGH, PRABHLEEN · 2010 to 2014
$760k
NIDDK NIH HHS K08 DK084305NIDDK NIH HHS P30 DK063491
6 · The paper itself

Abstract

BACKGROUND/

aimsAcute kidney injury (AKI) contributes to significant morbidity and mortality in the intensive care unit (ICU). Plasma levels of interleukin (IL)-6 predict the development of AKI and are associated with higher mortality in ICU patients with AKI. Most studies in AKI have focused on the tubulo-interstitium, despite evidence of glomerular involvement. In the following study, our goals were to investigate the expression of IL-6 and its downstream mediators in septic-induced AKI.

methodsPodocytes were treated in vitro with lipopolysaccharide (LPS) and mice were treated with LPS, and we evaluated IL-6 expression by real-time PCR, ELISA and in situ RNA hybridization.

resultsFollowing LPS stimulation, IL-6 is rapidly and highly induced in cultured podocytes and in vivo in glomeruli and infiltrating leukocytes. Surprisingly, in direct response to exogenous IL-6, podocytes produce lipocalin-2/neutrophil gelatinase-associated lipocalin (Lcn2/Ngal). LPS also potently induces Lcn2/Ngal expression in podocytes in culture and in glomeruli in vivo. Intense Lcn2/Ngal expression is also observed in IL-6 knockout mice, suggesting that while IL-6 may be sufficient to induce glomerular Lcn2/Ngal expression, it is not essential.

conclusionsThe glomerulus is involved in septic AKI, and we demonstrate that podocytes secrete key mediators of AKI including IL-6 and Lcn2/Ngal.

Indexed as

Acute Kidney InjuryAcute-Phase ProteinsAnimalsCell Line, TransformedCells, CulturedInterleukin-6Kidney GlomerulusLipocalin-2LipocalinsLipopolysaccharidesMiceMice, Inbred C57BLMice, KnockoutOncogene ProteinsPodocytesAcute-Phase ProteinsInterleukin-6interleukin-6, mouseLcn2 protein, mouseLipocalin-2LipocalinsLipopolysaccharidesOncogene Proteins

Identifiers

PMID23234871
PMCPMC4012854
OpenAlexW1970509998

What Socratic holds

Textmetadata
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 Socratic graph.