Evidence map›Paper›PMID 23359116›Full record

ArticlePloS one2013

Glomerular endothelial cell injury and damage precedes that of podocytes in adriamycin-induced nephropathy.

Yu Bo Yang Sun, Xinli Qu, Xueming Zhang, Georgina Caruana, John F Bertram, Jinhua Li

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 75 papers.

0numbers the graph read from it
0cells of the map it votes in
75citing papers in PubMed
5.3field-weighted citation impact, top 4% 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

75 citing papers in PubMed, 119 citations in OpenAlex.

  1. Article
  2. The endothelium response to kidney injury.Nature reviews. Nephrology · 2026
    Review
  3. Article
  4. Article
  5. Article
  6. Review
  7. Review
  8. Article
  9. Review
  10. Research (Washington, D.C.) · 2025
    Article
  11. Review
  12. Inflammation in glomerular diseases.Frontiers in immunology · 2025
    Review
  13. Article
  14. Review
  15. Non-voltage-gated CaAmerican journal of physiology. Renal physiology · 2024
    Review
  16. Article
  17. Review
  18. Review
  19. Article
  20. Molecular pathways that drive diabetic kidney disease.The Journal of clinical investigation · 2023
    Review

15 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

6 authors at 2 institutions in 2 countries.

Yu Bo Yang SunDepartment of Anatomy and Developmental Biology, Monash University, Wellington Road, Clayton, Victoria, Australia.
Xinli Qu
Xueming Zhang
Georgina Caruana
John F Bertram
Jinhua Li
Monash University · AUInner Mongolia University of Science and Technology · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The role of podocytes in the development and progression of glomerular disease has been extensively investigated in the past decade. However, the importance of glomerular endothelial cells in the pathogenesis of proteinuria and glomerulosclerosis has been largely ignored. Recent studies have demonstrated that endothelial nitric oxide synthatase (eNOS) deficiency exacerbates renal injury in anti-GBM and remnant kidney models and accelerates diabetic kidney damage. Increasing evidence also demonstrates the importance of the glomerular endothelium in preventing proteinuria. We hypothesize that endothelial dysfunction can initiate and promote the development and progression of glomerulopathy. Administration of adriamycin (ADR) to C57BL/6 mice, normally an ADR resistant strain, with an eNOS deficiency induced overt proteinuria, severe glomerulosclerosis, interstitial fibrosis and inflammation. We also examined glomerular endothelial cell and podocyte injury in ADR-induced nephropathy in Balb/c mice, an ADR susceptible strain, by immunostaining, TUNEL and Western blotting. Interestingly, down-regulation of eNOS and the appearance of apoptotic glomerular endothelial cells occurred as early as 24 hours after ADR injection, whilst synaptopodin, a functional podocyte marker, was reduced 7 days after ADR injection and coincided with a significant increase in the number of apoptotic podocytes. Furthermore, conditioned media from mouse microvascular endothelial cells over-expressing GFP-eNOS protected podocytes from TNF-α-induced loss of synaptopodin. In conclusion, our study demonstrated that endothelial dysfunction and damage precedes podocyte injury in ADR-induced nephropathy. Glomerular endothelial cells may protect podocytes from inflammatory insult. Understanding the role of glomerular endothelial dysfunction in the development of kidney disease will facilitate in the design of novel strategies to treat kidney disease.

Indexed as

AnimalsBlotting, WesternCulture Media, ConditionedDoxorubicinEndothelium, VascularIn Situ Nick-End LabelingKidneyKidney GlomerulusMiceMice, Inbred BALB CMice, Inbred C57BLMicroscopy, ConfocalNitric Oxide Synthase Type IIIPodocytesCulture Media, ConditionedDoxorubicinNitric Oxide Synthase Type III

Identifiers

PMID23359116
PMCPMC3554670
OpenAlexW2051659273

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.