Evidence map›Paper›PMID 23364805›Full record

ArticleAmerican journal of physiology. Renal physiology2013

Inhibition of p38 MAPK attenuates renal atrophy and fibrosis in a murine renal artery stenosis model.

Diping Wang, Gina M Warner, Ping Yin, Bruce E Knudsen, Jingfei Cheng, Kim A Butters, Karen R Lien, Catherine E Gray, Vesna D Garovic, Lilach O Lerman and 4 more

Open access · greenAbstract read
In one paragraph

Article in American journal of physiology. Renal physiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed
5.7field-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

35 citing papers in PubMed, 55 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Review
  17. Article
  18. Emerging Paradigms in Chronic Kidney Ischemia.Hypertension (Dallas, Tex. : 1979) · 2018
    Review
  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

14 authors at 1 institution in 1 country.

Diping WangDepartment of Laboratory Medicine and Pathology, Mayo Clinic, Rochester, MN 55905, USA.
Gina M Warner
Ping Yin
Bruce E Knudsen
Jingfei Cheng
Kim A Butters
Karen R Lien
Catherine E Gray
Vesna D Garovic
Lilach O Lerman
Stephen C Textor
Karl A Nath
Robert D Simari
Joseph P Grande
Mayo Clinic · US

Funding

MAYO CLINIC CENTER FOR TRANSLATIONAL SCIENCE ACTIVITIESUL1RR024150 · NCRR · MAYO CLINIC ROCHESTER · PI RIZZA, ROBERT A. · 2006 to 2011
$66.4M
Tissue Oxygenation in Human Renovascular HypertensionP01HL085307 · NHLBI · MAYO CLINIC ROCHESTER · PI ROMERO, JUAN C · 2007 to 2011
$10.4M
KIDNEY DISEASES RESEARCH TRAINING PROGRAMT32DK007013 · NIDDK · MAYO CLINIC ROCHESTER · PI LIESKE, JOHN C · 1986 to 2023
$3.7M
NCRR NIH HHS UL1-RR024150NHLBI NIH HHS P01-HL-85307NIDDK NIH HHS DK-007013-35
6 · The paper itself

Abstract

Renal artery stenosis (RAS) is an important cause of chronic renal dysfunction. Recent studies have underscored a critical role for CCL2 (MCP-1)-mediated inflammation in the progression of chronic renal damage in RAS and other chronic renal diseases. In vitro studies have implicated p38 MAPK as a critical intermediate for the production of CCL2. However, a potential role of p38 signaling in the development and progression of chronic renal disease in RAS has not been previously defined. We sought to test the hypothesis that inhibition of p38 MAPK ameliorates chronic renal injury in mice with RAS. We established a murine RAS model by placing a cuff on the right renal artery and treated mice with the p38 inhibitor SB203580 or vehicle for 2 wk. In mice treated with vehicle, the cuffed kidney developed interstitial fibrosis, tubular atrophy, and interstitial inflammation. In mice treated with SB203580, the RAS-induced renal atrophy was reduced (70% vs. 39%, P < 0.05). SB203580 also reduced interstitial inflammation and extracellular matrix deposition but had no effect on the development of hypertension. SB203580 partially blocked the induction of CCL2, CCL7 (MCP-3), CC chemokine receptor 2 (CCR2), and collagen 4 mRNA expression in the cuffed kidneys. In vitro, blockade of p38 hindered both TNF-α and TGF-β-induced CCL2 upregulation. Based on these observations, we conclude that p38 MAPK plays a critical role in the induction of CCL2/CCL7/CCR2 system and the development of interstitial inflammation in RAS.

Indexed as

AnimalsAtrophyChemokine CCL2Chemokine CCL7Disease Models, AnimalFibrosisImidazolesKidneyMaleMiceMice, Inbred C57BLNephrosclerosisp38 Mitogen-Activated Protein KinasesPyridinesReceptors, CCR2Renal Artery ObstructionCcl2 protein, mouseCcl7 protein, mouseCcr2 protein, mouseChemokine CCL2Chemokine CCL7Imidazolesp38 Mitogen-Activated Protein KinasesPyridinesReceptors, CCR2SB 203580

Identifiers

PMID23364805
PMCPMC3625852
OpenAlexW2155738377

What OpenQuestion holds

Textmetadata
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.