Evidence map›Paper›PMID 29609537›Full record

ArticleBMC nephrology2018

No difference in renal injury and fibrosis between wild-type and NOD1/NOD2 double knockout mice with chronic kidney disease induced by ureteral obstruction.

Ingrid Stroo, Diba Emal, Loes M Butter, Gwen J Teske, Nike Claessen, Mark C Dessing, Stephen E Girardin, Sandrine Florquin, Jaklien C Leemans

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in BMC nephrology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.5field-weighted citation impact, top 38% 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

4 citing papers in PubMed, 7 citations in OpenAlex.

  1. Genetic Deletion of NOD1 Prevents Cardiac CaInternational journal of molecular sciences · 2020
    Article
  2. Article
  3. The Impact of theBioMed research international · 2020
    Article
  4. 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.

Ingrid StrooDepartment of Pathology, Academic Medical Center, University of Amsterdam, Meibergdreef 9, room L2-112, 1105, AZ, Amsterdam, The Netherlands.
Diba EmalDepartment of Pathology, Academic Medical Center, University of Amsterdam, Meibergdreef 9, room L2-112, 1105, AZ, Amsterdam, The Netherlands. d.emal@amc.uva.nl.
Loes M ButterDepartment of Pathology, Academic Medical Center, University of Amsterdam, Meibergdreef 9, room L2-112, 1105, AZ, Amsterdam, The Netherlands.
Gwen J TeskeDepartment of Pathology, Academic Medical Center, University of Amsterdam, Meibergdreef 9, room L2-112, 1105, AZ, Amsterdam, The Netherlands.
Nike ClaessenDepartment of Pathology, Academic Medical Center, University of Amsterdam, Meibergdreef 9, room L2-112, 1105, AZ, Amsterdam, The Netherlands.
Mark C DessingDepartment of Pathology, Academic Medical Center, University of Amsterdam, Meibergdreef 9, room L2-112, 1105, AZ, Amsterdam, The Netherlands.
Stephen E GirardinDepartment of Laboratory Medicine and Pathobiology, University of Toronto, Toronto, Canada.
Sandrine FlorquinDepartment of Pathology, Academic Medical Center, University of Amsterdam, Meibergdreef 9, room L2-112, 1105, AZ, Amsterdam, The Netherlands.
Jaklien C LeemansDepartment of Pathology, Academic Medical Center, University of Amsterdam, Meibergdreef 9, room L2-112, 1105, AZ, Amsterdam, The Netherlands.
Academic Medical Center · NLUniversity of Amsterdam · NLUniversity of Toronto · CA

Funding

CIHR
6 · The paper itself

Abstract

backgroundChronic kidney disease (CKD) is characterized by sustained tissue damage and ongoing tubulo-interstitial inflammation and fibrosis. Pattern recognition receptors (PRRs) including Toll-like receptors (TLRs) and NOD-like receptors (NLRs) can sense endogenous ligands released upon tissue damage, leading to sterile inflammation and eventually irreversible kidney disease. It is known that NOD1 and NOD2 contribute to the pathogenesis of various inflammatory diseases, including acute kidney injury. However their role in chronic kidney disease is largely unknown. The aim of this study was therefore to investigate the contribution of NOD1 and NOD2 in renal interstitial fibrosis and obstructive nephropathy.

methodsTo do so, we performed unilateral ureteral obstruction (UUO) in wild type (WT) and NOD1/NOD2 double deficient (DKO) mice and analysed renal damage, fibrosis and inflammation. Data were analysed using the non-parametric Mann-Whitney U-test.

resultsMinor changes in inflammatory response were observed in NOD1/2 DKO mice, while no effects were observed on renal injury and the development of fibrosis.

conclusionNo difference in renal injury and fibrosis between WT and NOD1/NOD2 DKO mice following obstructive nephropathy induced by ureteral obstruction.

Indexed as

Acute Kidney InjuryAnimalsFemaleFibrosisMiceMice, Inbred C57BLMice, Inbred NODMice, KnockoutNod1 Signaling Adaptor ProteinNod2 Signaling Adaptor ProteinRenal Insufficiency, ChronicUreteral ObstructionNod1 protein, mouseNod1 Signaling Adaptor ProteinNod2 protein, mouseNod2 Signaling Adaptor ProteinNOD1NOD2Obstructive nephropathyPattern recognition receptorsRenal fibrosis

Identifiers

PMID29609537
PMCPMC5879837
OpenAlexW2804311153

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.