Evidence map›Paper›PMID 18458097›Full record

ArticleThe American journal of pathology2008

L-arginine decreases inflammation and modulates the nuclear factor-kappaB/matrix metalloproteinase cascade in mdx muscle fibers.

Karim Hnia, Jérôme Gayraud, Gérald Hugon, Michèle Ramonatxo, Sabine De La Porte, Stefan Matecki, Dominique Mornet

Open access · bronzeAbstract read
In one paragraph

Article in The American journal of pathology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 96 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
96citing papers in PubMed, 2 pooled it
7.0field-weighted citation impact, top 2% 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

96 citing papers in PubMed, 2 syntheses or guidelines pooled it, 169 citations in OpenAlex.

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  19. Effects ofFrontiers in microbiology · 2024
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36 more citing papers are in PubMed but not listed here.

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 3 institutions in 1 country.

Karim HniaINSERM ERI 25 Muscle et Pathologies, CHU A. de Villeneuve, Université de Montpellier1, EA 4202, 34295 Montpellier Cedex 5, France.
Jérôme Gayraud
Gérald Hugon
Michèle Ramonatxo
Sabine De La Porte
Stefan Matecki
Dominique Mornet
Inserm · FRUniversité de Montpellier · FRLaboratoire de Neurobiologie Cellulaire et Moléculaire · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Duchenne muscular dystrophy (DMD) is a lethal, X-linked disorder associated with dystrophin deficiency that results in chronic inflammation, sarcolemma damage, and severe skeletal muscle degeneration. Recently, the use of L-arginine, the substrate of nitric oxide synthase (nNOS), has been proposed as a pharmacological treatment to attenuate the dystrophic pattern of DMD. However, little is known about signaling events that occur in dystrophic muscle with l-arginine treatment. Considering the implication of inflammation in dystrophic processes, we asked whether L-arginine inhibits inflammatory signaling cascades. We demonstrate that L-arginine decreases inflammation and enhances muscle regeneration in the mdx mouse model. Classic stimulatory signals, such as proinflammatory cytokines interleukin-1beta, interleukin-6, and tumor necrosis factor-alpha, are significantly decreased in mdx mouse muscle, resulting in lower nuclear factor (NF)-kappaB levels and activity. NF-kappaB serves as a pivotal transcription factor with multiple levels of regulation; previous studies have shown perturbation of NF-kappaB signaling in both mdx and DMD muscle. Moreover, L-arginine decreases the activity of metalloproteinase (MMP)-2 and MMP-9, which are transcriptionally activated by NF-kappaB. We show that the inhibitory effect of L-arginine on the NF-kappaB/MMP cascade reduces beta-dystroglycan cleavage and translocates utrophin and nNOS throughout the sarcolemma. Collectively, our results clarify the molecular events by which L-arginine promotes muscle membrane integrity in dystrophic muscle and suggest that NF-kappaB-related signaling cascades could be potential therapeutic targets for DMD management.

Indexed as

AnimalsArginineInflammationMAP Kinase Signaling SystemMatrix Metalloproteinase 2Matrix Metalloproteinase 9MiceMice, Inbred mdxMuscle Fibers, SkeletalMuscle, SkeletalMuscular Dystrophy, DuchenneNF-kappa BNitric Oxide SynthaseRegenerationSignal TransductionArginineMatrix Metalloproteinase 2Matrix Metalloproteinase 9Mmp2 protein, mouseMmp9 protein, mouseNF-kappa BNitric Oxide Synthase

Identifiers

PMID18458097
PMCPMC2408412
OpenAlexW2035841380

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.