Evidence map›Paper›PMID 31043586›Full record

ArticleCell death & disease2019

nNOS/GSNOR interaction contributes to skeletal muscle differentiation and homeostasis.

Costanza Montagna, Salvatore Rizza, Claudia Cirotti, Emiliano Maiani, Maurizio Muscaritoli, Antonio Musarò, Maria Teresa Carrí, Elisabetta Ferraro, Francesco Cecconi, Giuseppe Filomeni

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
0.7field-weighted citation impact, top 31% 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

9 citing papers in PubMed, 19 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Article
  6. Review
  7. Autophagy guards tendon homeostasis.Cell death & disease · 2022
    Article
  8. Review
  9. Can Serum Nitrosoproteome Predict Longevity of Aged Women?International journal of molecular sciences · 2020
    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

10 authors at 5 institutions in 2 countries.

Costanza MontagnaCell Stress and Survival Unit, Danish Cancer Society Research Center, 2100, Copenhagen, Denmark.
Salvatore RizzaCell Stress and Survival Unit, Danish Cancer Society Research Center, 2100, Copenhagen, Denmark.ORCID http://orcid.org/0000-0001-7335-4684
Claudia CirottiDepartment of Biology, Tor Vergata University of Rome, 00133, Rome, Italy.
Emiliano MaianiCell Stress and Survival Unit, Danish Cancer Society Research Center, 2100, Copenhagen, Denmark.
Maurizio MuscaritoliDepartment of Translational and Precision Medicine (formerly Department of Clinical Medicine), Sapienza University of Rome, 00185, Rome, Italy.
Antonio MusaròDAHFMO-Unit of Histology and Medical Embryology, Sapienza University of Rome, 00161, Rome, Italy.ORCID http://orcid.org/0000-0002-2944-9739
Maria Teresa CarríDepartment of Biology, Tor Vergata University of Rome, 00133, Rome, Italy.
Elisabetta FerraroDepartment of Orthopaedics and Traumatology, Hospital "Maggiore della Carità", University of Piemonte Orientale (UPO), Novara, Italy.
Francesco CecconiCell Stress and Survival Unit, Danish Cancer Society Research Center, 2100, Copenhagen, Denmark.ORCID http://orcid.org/0000-0002-5614-4359
Giuseppe FilomeniCell Stress and Survival Unit, Danish Cancer Society Research Center, 2100, Copenhagen, Denmark. giufil@cancer.dk.
University of Rome Tor Vergata · ITDanish Cancer Society · DKSapienza University of Rome · ITBispebjerg Hospital · DKUniversità degli Studi del Piemonte Orientale “Amedeo Avogadro” · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Neuronal nitric oxide synthase (nNOS) plays a crucial role in the maintenance of correct skeletal muscle function due, at least in part, to S-nitrosylation of specific protein targets. Similarly, we recently provided evidence for a muscular phenotype in mice lacking the denitrosylase S-nitrosoglutathione reductase (GSNOR). Here, we demonstrate that nNOS and GSNOR are concomitantly expressed during differentiation of C2C12. They colocalizes at the sarcolemma and co-immunoprecipitate in cells and in myofibers. We also provide evidence that GSNOR expression decreases in mouse models of muscular dystrophies and of muscle atrophy and wasting, i.e., aging and amyotrophic lateral sclerosis, suggesting a more general regulatory role of GSNOR in skeletal muscle homeostasis.

Indexed as

AgingAlcohol DehydrogenaseAnimalsCell DifferentiationCell Line, TransformedDisease Models, AnimalDystrophin-Associated ProteinsGene Expression RegulationHomeostasisHumansMiceMice, Inbred mdxMice, KnockoutMuscle DevelopmentMuscle, SkeletalMuscular DystrophiesAdh5 protein, mouseAlcohol DehydrogenaseDystrophin-Associated ProteinsNitric OxideNitric Oxide Synthase Type INos1 protein, mouseRNA, Small InterferingSod1 protein, mouseSuperoxide Dismutase-1syntrophin

Identifiers

PMID31043586
PMCPMC6494884
OpenAlexW2943278113

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.