Evidence map›Paper›PMID 27914709›Full record

ArticleKidney international2017

Podocyte-specific chemokine (C-C motif) receptor 2 overexpression mediates diabetic renal injury in mice.

Hanning You, Ting Gao, Wesley M Raup-Konsavage, Timothy K Cooper, Sarah K Bronson, W Brian Reeves, Alaa S Awad

Open access · bronzeAbstract read
In one paragraph

Article in Kidney international, 2017. 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
2.7field-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

19 citing papers in PubMed, 46 citations in OpenAlex.

  1. Trial
  2. Article
  3. Review
  4. Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Mechanisms of podocyte injury and implications for diabetic nephropathy.Clinical science (London, England : 1979) · 2022
    Article
  10. Article
  11. Article
  12. The Role of Chemokines and Chemokine Receptors in Diabetic Nephropathy.International journal of molecular sciences · 2020
    Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Role of Podocyte Injury in Glomerulosclerosis.Advances in experimental medicine and biology · 2019
    Review
  18. Acute Kidney Injury and Progression of Diabetic Kidney Disease.Advances in chronic kidney disease · 2018
    Review
  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

7 authors at 2 institutions in 1 country.

Hanning YouDepartment of Medicine, Penn State University College of Medicine, Hershey, Pennsylvania, USA.
Ting GaoDepartment of Medicine, Penn State University College of Medicine, Hershey, Pennsylvania, USA.
Wesley M Raup-KonsavageDepartment of Medicine, Penn State University College of Medicine, Hershey, Pennsylvania, USA.
Timothy K CooperDepartment of Comparative Medicine, Penn State University College of Medicine, Hershey, Pennsylvania, USA.
Sarah K BronsonDepartment of Cellular and Molecular Physiology, Penn State University College of Medicine, Hershey, Pennsylvania, USA.
W Brian ReevesDepartment of Medicine, Penn State University College of Medicine, Hershey, Pennsylvania, USA.
Alaa S AwadDepartment of Medicine, Penn State University College of Medicine, Hershey, Pennsylvania, USA; Department of Cellular and Molecular Physiology, Penn State University College of Medicine, Hershey, Pennsylvania, USA. Electronic address: asa17@psu.edu.
Penn State Milton S. Hershey Medical Center · USPennsylvania State University · US

Funding

Role of Arginase in Diabetic NephropathyR01DK094930 · NIDDK · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI AWAD, ALAA S · 2012 to 2016
$1.9M
TRPM2 in Ischemic AKIR01DK108185 · NIDDK · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI REEVES, WILLIAM BRIAN · 2016 to 2019
$1.7M
NIDDK NIH HHS R01 DK094930NIDDK NIH HHS R01 DK108185
6 · The paper itself

Abstract

Inflammation is a central pathophysiologic mechanism that contributes to diabetes mellitus and diabetic nephropathy. Recently, we showed that macrophages directly contribute to diabetic renal injury and that pharmacological blockade or genetic deficiency of chemokine (C-C motif) receptor 2 (CCR2) confers kidney protection in diabetic nephropathy. However, the direct role of CCR2 in kidney-derived cells such as podocytes in diabetic nephropathy remains unclear. To study this, we developed a transgenic mouse model expressing CCR2 specifically in podocytes (Tg[NPHS2-Ccr2]) on a nephropathy-prone (DBA/2J) and CCR2-deficient (Ccr2

Indexed as

AlbuminuriaAnimalsApoptosisBlood Urea NitrogenCollagen Type IDiabetes Mellitus, ExperimentalDiabetes Mellitus, Type 1Diabetic NephropathiesFibronectinsFibrosisGenetic Predisposition to DiseaseInflammation MediatorsMacrophagesMaleMice, Inbred DBAMice, KnockoutCcr2 protein, mouseCollagen Type IFibronectinsInflammation MediatorsReceptors, CCR2RNA, MessengerStreptozocinCCR2diabetic nephropathypodocytes

Identifiers

PMID27914709
PMCPMC5313320
OpenAlexW2559144666

What Socratic holds

Textmetadata
LicenceTDM
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.