Evidence map›Paper›PMID 30254418›Full record

ArticleDrug design, development and therapy2018

Inhibitor of IGF1 receptor alleviates the inflammation process in the diabetic kidney mouse model without activating SOCS2.

Jiayu Li, Rong Dong, Jiali Yu, Sun Yi, Jingjing Da, Fuxun Yu, Yan Zha

Open access · goldAbstract read
In one paragraph

Article in Drug design, development and therapy, 2018. 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
1.1field-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

21 citing papers in PubMed, 33 citations in OpenAlex.

  1. Trial
  2. Article
  3. Article
  4. Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  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

7 authors at 2 institutions in 1 country.

Jiayu LiGuizhou University School of Medicine, Guizhou University.
Rong DongDepartment of Nephrology, Guizhou Provincial People's Hospital, yanzha72@yeah.net.
Jiali YuDepartment of Nephrology, Guizhou Provincial People's Hospital, yanzha72@yeah.net.
Sun YiDepartment of Nephrology, Guizhou Provincial People's Hospital, yanzha72@yeah.net.
Jingjing DaDepartment of Nephrology, Guizhou Provincial People's Hospital, yanzha72@yeah.net.
Fuxun YuDepartment of Central Laboratory, Guizhou Provincial People's Hospital, Guiyang, China.
Yan ZhaDepartment of Nephrology, Guizhou Provincial People's Hospital, yanzha72@yeah.net.
Guizhou Provincial People's Hospital · CNGuizhou University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveTo explore the anti-inflammatory mechanism of IGF1R inhibitor in diabetic nephropathy.

methodsC57/BL6 mice were reared with high-fat diet for 8 weeks, then were injected 30 mg/kg streptozotocin intraperitoneally to induce type 2 diabetes. After 8 weeks, the type 2 diabetes nephropathy model was successfully set up the different drugs were administrated to mice with diabetes (insulin 1-2 U/day, benazepril 10 mg/kg per day intragastrically, IGF-1R inhibitor 30 mg/kg per day intragastrically). After 8 weeks drugs administration, all mice were collected the kidney tissue, measured levels of inflammatory factor (F4/80, TLR4and CD68) and fibrosis markers(αSMA, E-cadherin and SR) using immunohistochemistry and in situ hybridization.

resultsThe type 2 diabetes nephropathy model was built successfully, which along with increased urinary protein excretion rate and increased inflammatory infiltration, and the correlation was characterized by increased CD68

conclusionInhibition of IGF1R was a more effective choice for inflammation treatment than Ben or Ins in diabetic kidney disease (DKD). The IGF1R inhibitor blocked pathological changes induced by the over-expression of IGF1 in DKD without up-regulating SOCS2 protein levels.

Indexed as

Disease Models, AnimalAnimalsAnti-Inflammatory Agents, Non-SteroidalDiabetes Mellitus, ExperimentalDiabetes Mellitus, Type 2Diabetic NephropathiesImidazolesInflammationInjections, IntraperitonealMaleMiceMice, Inbred C57BLPyridinesReceptor, IGF Type 1StreptozocinSuppressor of Cytokine Signaling ProteinsAnti-Inflammatory Agents, Non-SteroidalGSK1904529AImidazolesPyridinesReceptor, IGF Type 1Socs2 protein, mouseStreptozocinSuppressor of Cytokine Signaling Proteinsdiabetes kidney diseaseIGF1R inhibitorinsulinSOCS2

Identifiers

PMID30254418
PMCPMC6141121
OpenAlexW2891569342

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.