Evidence map›Paper›PMID 24167558›Full record

ArticlePloS one2013

G-CSF prevents progression of diabetic nephropathy in rat.

Byung-Im So, Yi-Sun Song, Cheng-Hu Fang, Jun-Young Park, Yonggu Lee, Jeong Hun Shin, Hyuck Kim, Kyung-Soo Kim

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 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.4field-weighted citation impact, top 20% 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

13 citing papers in PubMed, 19 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Accelerated Kidney Aging in Diabetes Mellitus.Oxidative medicine and cellular longevity · 2020
    Review
  5. Review
  6. Article
  7. Evidence-based complementary and alternative medicine : eCAM · 2019
    Article
  8. JYYS Granule Mitigates Renal Injury in Clinic and in Spontaneously Hypertensive Rats by Inhibiting NF-Evidence-based complementary and alternative medicine : eCAM · 2018
    Article
  9. Article
  10. FK506 reduces albuminuria through improving podocyte nephrin and podocin expression in diabetic rats.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2016
    Article
  11. Article
  12. Article
  13. 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

8 authors at 2 institutions in 2 countries.

Byung-Im SoGraduate School of Biomedical Science and Engineering, Hanyang University, Seoul, Korea.
Yi-Sun Song
Cheng-Hu Fang
Jun-Young Park
Yonggu Lee
Jeong Hun Shin
Hyuck Kim
Kyung-Soo Kim
Hanyang University · KRYanbian University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThe protective effects of granulocyte colony-stimulating factor (G-CSF) have been demonstrated in a variety of renal disease models. However, the influence of G-CSF on diabetic nephropathy (DN) remains to be examined. In this study, we investigated the effect of G-CSF on DN and its possible mechanisms in a rat model.

methodsOtsuka Long-Evans Tokushima Fatty (OLETF) rats with early DN were administered G-CSF or saline intraperitoneally. Urine albumin creatinine ratio (UACR), creatinine clearance, mesangial matrix expansion, glomerular basement membrane (GBM) thickness, and podocyte foot process width (FPW) were measured. The levels of interleukin (IL)-1β, transforming growth factor (TGF)-β1, and type IV collagen genes expression in kidney tissue were also evaluated. To elucidate the mechanisms underlying G-CSF effects, we also assessed the expression of G-CSF receptor (G-CSFR) in glomeruli as well as mobilization of bone marrow (BM) cells to glomeruli using sex-mismatched BM transplantation.

resultsAfter four weeks of treatment, UACR was lower in the G-CSF treatment group than in the saline group (p<0.05), as were mesangial matrix expansion, GBM thickness, and FPW (p<0.05). In addition, the expression of TGF-β1 and type IV collagen and IL-1β levels was lower in the G-CSF treatment group (p<0.05). G-CSFR was not present in glomerular cells, and G-CSF treatment increased the number of BM-derived cells in glomeruli (p<0.05).

conclusionsG-CSF can prevent the progression of DN in OLETF rats and its effects may be due to mobilization of BM cells rather than being a direct effect.

Indexed as

AllograftsAnimalsBone Marrow CellsBone Marrow TransplantationCell MovementCollagen Type VIDiabetes Mellitus, ExperimentalDiabetic NephropathiesGene Expression RegulationGlomerular Basement MembraneGlomerular Filtration RateGranulocyte Colony-Stimulating FactorInterleukin-1betaPodocytesRatsRats, Inbred OLETFCollagen Type VIGranulocyte Colony-Stimulating FactorInterleukin-1betaTransforming Growth Factor beta1

Identifiers

PMID24167558
PMCPMC3805566
OpenAlexW1979102578

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.