Evidence map›Paper›PMID 23071743›Full record

ArticlePloS one2012

A purpose-synthesised anti-fibrotic agent attenuates experimental kidney diseases in the rat.

Richard E Gilbert, Yuan Zhang, Spencer J Williams, Steven C Zammit, David I Stapleton, Alison J Cox, Henry Krum, Robyn Langham, Darren J Kelly

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
2.7field-weighted citation impact, top 10% 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

21 citing papers in PubMed, 43 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Review
  5. Article
  6. Article
  7. Article
  8. Review
  9. Article
  10. Review
  11. Article
  12. Therapeutic targets for treating fibrotic kidney diseases.Translational research : the journal of laboratory and clinical medicine · 2015
    Review
  13. Article
  14. Article
  15. Article
  16. Review
  17. The endothelium in diabetic nephropathy.Current atherosclerosis reports · 2014
    Review
  18. Article
  19. Diabetic nephropathy: diagnosis and treatment.Nature reviews. Endocrinology · 2013
    Review
  20. 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 3 institutions in 2 countries.

Richard E GilbertKeenan Research Centre, Li Ka Shing Knowledge Institute, St. Michael's Hospital, Toronto, Ontario, Canada. richard.gilbert@utoronto.ca
Yuan Zhang
Spencer J Williams
Steven C Zammit
David I Stapleton
Alison J Cox
Henry Krum
Robyn Langham
Darren J Kelly
University of Melbourne · AUMonash University · AUSt. Michael's Hospital · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

background and purposeLocally-active growth factors have been implicated in the pathogenesis of many diseases in which organ fibrosis is a characteristic feature. In the setting of chronic kidney disease (CKD), two such pro-fibrotic factors, transforming growth factor-β (TGF-β) and platelet-derived growth factor (PDGF) have emerged as lead potential targets for intervention. Given the incomplete organ protection afforded by blocking the actions of TGF-β or PDGF individually, we sought to determine whether an agent that inhibited the actions of both may have broader effects in ameliorating the key structural and functional abnormalities of CKD. EXPERIMENTAL APPROACH: Accordingly, we studied the effects of a recently described, small molecule anti-fibrotic drug, 3-methoxy-4-propargyloxycinnamoyl anthranilate (FT011, Fibrotech Therapeutics, Australia), which should have these effects. KEY

resultsIn the in vitro setting, FT011 inhibited both TGF-β1 and PDGF-BB induced collagen production as well as PDGF-BB-mediated mesangial proliferation. Consistent with these in vitro actions, when studied in a robust model of non-diabetic kidney disease, the 5/6 nephrectomised rat, FT011 attenuated the decline in GFR, proteinuria and glomerulosclerosis (p<0.05 for all). Similarly, in the streptozotocin-diabetic Ren-2 rat, a model of advanced diabetic nephropathy, FT011 reduced albuminuria, glomerulosclerosis and tubulointerstitial fibrosis. CONCLUSIONS AND IMPLICATIONS: Together these studies suggest that broadly antagonising growth factor actions, including those of TGF-β1 and PDGF-BB, has the potential to protect the kidney from progressive injury in both the diabetic and non-diabetic settings.

Indexed as

AlbuminuriaAnimalsBecaplerminCaffeic AcidsCell ProliferationCells, CulturedCollagenDiabetes Mellitus, ExperimentalDisease Models, AnimalFemaleMacrophagesMaleMesangial Cellsortho-AminobenzoatesOsteopontinProtective Agents3-methoxy-4-propargyloxycinnamoyl anthranilateBecaplerminCaffeic AcidsCollagenortho-AminobenzoatesOsteopontinProtective AgentsProto-Oncogene Proteins c-sisTransforming Growth Factor beta1

Identifiers

PMID23071743
PMCPMC3468513
OpenAlexW1972887649

What OpenQuestion holds

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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.