Evidence map›Paper›PMID 26367310›Full record

ArticlePloS one2015

Reduced NOV/CCN3 Expression Limits Inflammation and Interstitial Renal Fibrosis after Obstructive Nephropathy in Mice.

Pierre-Olivier Marchal, Panagiotis Kavvadas, Ahmed Abed, Chantal Kazazian, Florence Authier, Haruhiko Koseki, Shuichi Hiraoka, Jean-Jacques Boffa, Cécile Martinerie, Christos E Chadjichristos

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed, 1 pooled it
2.0field-weighted citation impact, top 13% 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

20 citing papers in PubMed, 1 synthesis or guideline pooled it, 33 citations in OpenAlex.

  1. Pooled it
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  5. The advance of CCN3 in fibrosis.Journal of cell communication and signaling · 2023
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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

10 authors at 7 institutions in 2 countries.

Pierre-Olivier MarchalINSERM, UMR-S938, Centre de Recherche Saint-Antoine, Saint-Antoine Hospital, Paris, France; INSERM UMR-S1155, Tenon Hospital, Paris, France; Sorbonne Universités, UPMC Univ Paris 6, Paris, France.
Panagiotis KavvadasINSERM UMR-S1155, Tenon Hospital, Paris, France.
Ahmed AbedINSERM UMR-S1155, Tenon Hospital, Paris, France; Sorbonne Universités, UPMC Univ Paris 6, Paris, France.
Chantal KazazianINSERM, UMR-S938, Centre de Recherche Saint-Antoine, Saint-Antoine Hospital, Paris, France.
Florence AuthierINSERM UMR-S1155, Tenon Hospital, Paris, France.
Haruhiko KosekiRIKEN Research Center for Allergy and Immunology (RCAI), RIKEN Yokohama Institute, Yokohama, Japan.
Shuichi HiraokaDepartment of Biochemistry, Kobe Pharmaceutical University, Kobe, Japan.
Jean-Jacques BoffaINSERM UMR-S1155, Tenon Hospital, Paris, France; Department of Nephrology, Tenon Hospital, Paris, France.
Cécile MartinerieINSERM, UMR-S938, Centre de Recherche Saint-Antoine, Saint-Antoine Hospital, Paris, France; Sorbonne Universités, UPMC Univ Paris 6, Paris, France.
Christos E ChadjichristosINSERM UMR-S1155, Tenon Hospital, Paris, France; Sorbonne Universités, UPMC Univ Paris 6, Paris, France.
Hôpital Tenon · FRSorbonne Université · FRCentre de Recherche Saint-Antoine · FRDes Maladies Rénales Rares aux Maladies Fréquentes, Remodelage et Réparation · FRHôpital Saint-Antoine · FRKobe Pharmaceutical University · JPRIKEN Center for Integrative Medical Sciences · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The main hallmark of chronic kidney disease (CKD) is excessive inflammation leading to interstitial tissue fibrosis. It has been recently reported that NOV/CCN3 could be involved in kidney damage but its role in the progression of nephropathies is poorly known. NOV/CCN3 is a secreted multifunctional protein belonging to the CCN family involved in different physiological and pathological processes such as angiogenesis, inflammation and cancers. The purpose of our study was to determine the role of NOV/CCN3 in renal inflammation and fibrosis related to primitive tubulointerstitial injury. After unilateral ureteral obstruction (UUO), renal histology and real-time PCR were performed in NOV/CCN3-/- and wild type mice. NOV/CCN3 mRNA expression was increased in the obstructed kidneys in the early stages of the obstructive nephropathy. Interestingly, plasmatic levels of NOV/CCN3 were strongly induced after 7 days of UUO and the injection of recombinant NOV/CCN3 protein in healthy mice significantly increased CCL2 mRNA levels. Furthermore, after 7 days of UUO NOV/CCN3-/- mice displayed reduced proinflammatory cytokines and adhesion markers expression leading to restricted accumulation of interstitial monocytes, in comparison with their wild type littermates. Consequently, in NOV/CCN3-/- mice interstitial renal fibrosis was blunted after 15 days of UUO. In agreement with our experimental data, NOV/CCN3 expression was highly increased in biopsies of patients with tubulointerstitial nephritis. Thus, the inhibition of NOV/CCN3 may represent a novel target for the progression of renal diseases.

Indexed as

AnimalsBiomarkersFibrosisGene Expression RegulationHumansKidneyKidney DiseasesMaleMice, Inbred C57BLMice, Mutant StrainsNephritis, InterstitialNephroblastoma Overexpressed ProteinRenal Insufficiency, ChronicUreteral ObstructionBiomarkersCCN3 protein, humanCcn3 protein, mouseNephroblastoma Overexpressed Protein

Identifiers

PMID26367310
PMCPMC4569074
OpenAlexW2237741935

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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.