Evidence map›Paper›PMID 28832640›Full record

ArticlePloS one2017

Restored nitric oxide bioavailability reduces the severity of acute-to-chronic transition in a mouse model of aristolochic acid nephropathy.

Inès Jadot, Vanessa Colombaro, Blanche Martin, Isabelle Habsch, Olivia Botton, Joëlle Nortier, Anne-Emilie Declèves, Nathalie Caron

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
2.4field-weighted citation impact, top 12% 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

15 citing papers in PubMed, 32 citations in OpenAlex.

  1. Article
  2. Renal tubular epithelial IGFBP7 interacts with PKM2 to drive renal lipid accumulation and fibrosis.Molecular therapy : the journal of the American Society of Gene Therapy · 2025
    Article
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  10. Genome-wide transcriptional analysis ofPharmaceutical biology · 2020
    Article
  11. Article
  12. Review
  13. Article
  14. Article
  15. Rodent models of AKI-CKD transition.American journal of physiology. Renal physiology · 2018
    Review
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

8 authors at 3 institutions in 1 country.

Inès JadotMolecular Physiology Research Unit - URPhyM, NARILIS (Namur Research Institute for Life Sciences), University of Namur (UNamur), Namur, Belgium.ORCID http://orcid.org/0000-0002-4090-8385
Vanessa ColombaroMolecular Physiology Research Unit - URPhyM, NARILIS (Namur Research Institute for Life Sciences), University of Namur (UNamur), Namur, Belgium.
Blanche MartinMolecular Physiology Research Unit - URPhyM, NARILIS (Namur Research Institute for Life Sciences), University of Namur (UNamur), Namur, Belgium.
Isabelle HabschMolecular Physiology Research Unit - URPhyM, NARILIS (Namur Research Institute for Life Sciences), University of Namur (UNamur), Namur, Belgium.
Olivia BottonMolecular Physiology Research Unit - URPhyM, NARILIS (Namur Research Institute for Life Sciences), University of Namur (UNamur), Namur, Belgium.
Joëlle NortierNephrology Department, Erasme Academic Hospital and Laboratory of Experimental Nephrology, Faculty of Medicine, Université Libre de Bruxelles (ULB), Brussels, Belgium.
Anne-Emilie DeclèvesLaboratory of Molecular Biology, Faculty of Medicine and Pharmacy, Research Institute for Health Sciences and Technology, University of Mons (UMONS), Mons, Belgium.
Nathalie CaronMolecular Physiology Research Unit - URPhyM, NARILIS (Namur Research Institute for Life Sciences), University of Namur (UNamur), Namur, Belgium.
University of Namur · BEUniversité Libre de Bruxelles · BEUniversity of Mons · BE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Aristolochic Acid (AA) nephropathy (AAN) is a progressive tubulointerstitial nephritis characterized by an early phase of acute kidney injury (AKI) leading to chronic kidney disease (CKD). The reduced nitric oxide (NO) bioavailability reported in AAN might contribute to renal function impairment and progression of the disease. We previously demonstrated that L-arginine (L-Arg) supplementation is protective in AA-induced AKI. Since the severity of AKI may be considered a strong predictor of progression to CKD, the present study aims to assess the potential benefit of L-Arg supplementation during the transition from the acute phase to the chronic phase of AAN. C57BL/6J male mice were randomly subjected to daily i.p. injections of vehicle or AA for 4 days. To determine whether renal AA-induced injuries were linked to reduced NO production, L-Arg was added to drinking water from 7 days before starting i.p. injections, until the end of the protocol. Mice were euthanized 5, 10 and 20 days after vehicle or AA administration. AA-treated mice displayed marked renal injury and reduced NO bioavailability, while histopathological features of AAN were reproduced, including interstitial cell infiltration and tubulointerstitial fibrosis. L-Arg treatment restored renal NO bioavailability and reduced the severity of AA-induced injury, inflammation and fibrosis. We concluded that reduced renal NO bioavailability contributes to the processes underlying AAN. Furthermore, L-Arg shows nephroprotective effects by decreasing the severity of acute-to-chronic transition in experimental AAN and might represent a potential therapeutic tool in the future.

Indexed as

AnimalsArginineAristolochic AcidsBiological AvailabilityInflammationKidney DiseasesMiceNitric OxideArgininearistolochic acid IAristolochic AcidsNitric Oxide

Identifiers

PMID28832640
PMCPMC5568239
OpenAlexW2748517752

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

Registered trials

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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.