Evidence map›Paper›PMID 32751416›Full record

ArticleInternational journal of molecular sciences2020

Apocynin Treatment Prevents Cardiac Connexin 43 Hemichannels Hyperactivity by Reducing Nitroso-Redox Stress in Mdx Mice.

Alejandra Z Vielma, Mauricio P Boric, Daniel R Gonzalez

Open access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.2field-weighted citation impact, top 22% 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

14 citing papers in PubMed, 18 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Tetrahydrobiopterin (BHBiomedicines · 2022
    Article
  6. Review
  7. Review
  8. Review
  9. The mutual interplay of redox signaling and connexins.Journal of molecular medicine (Berlin, Germany) · 2021
    Review
  10. Peptidic Connexin43 Therapeutics in Cardiac Reparative Medicine.Journal of cardiovascular development and disease · 2021
    Review
  11. Article
  12. Importance of Cx43 for Right Ventricular Function.International journal of molecular sciences · 2021
    Review
  13. Review
  14. 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

3 authors at 2 institutions in 1 country.

Alejandra Z VielmaDepartamento de Fisiología, Facultad de Ciencias Biológicas, Pontificia Universidad Católica de Chile, Santiago 8320000, Chile.
Mauricio P BoricDepartamento de Fisiología, Facultad de Ciencias Biológicas, Pontificia Universidad Católica de Chile, Santiago 8320000, Chile.ORCID 0000-0001-6735-6675
Daniel R GonzalezDepartamento de Ciencias Básicas Biomédicas, Facultad de Ciencias de la Salud, Universidad de Talca, Talca 3460000, Chile.ORCID 0000-0002-3437-8998
Pontificia Universidad Católica de Chile · CLUniversity of Talca · CL

Funding

"NCD Training in CVD,pulmonary and obesity in Peru"D71TW011205 · FIC · ASOCIACION BENEFICA PRISMA · PI CHIANG, MARILU · 2018 to 2018
$50k
Fondo Nacional de Desarrollo Científico y Tecnológico 1120595
6 · The paper itself

Abstract

Duchenne muscular dystrophy (DMD) is a fatal disease that causes cardiomyopathy and is associated with oxidative stress. In the heart, oxidative stress interferes with the location of connexin 43 (Cx43) to the intercalated discs causing its lateralization to the plasma membrane where Cx43 forms hemichannels. We tested the hypothesis that in DMD cardiomyopathy, increased oxidative stress is associated with the formation and activation of Cx43 hemichannels. For this, we used mdx mice as a DMD model and evaluated cardiac function, nitroso-redox changes and Cx43 hemichannels permeability. Mdx hearts presented increased NADPH oxidase-derived oxidative stress and increased Cx43 S-nitrosylation compared to controls. These redox changes were associated with increased Cx43 lateralization, decreased cardiac contractility and increased arrhythmic events. Pharmacological inhibition of NADPH oxidase using apocynin (one month) reduced systemic oxidative stress and reversed the aforementioned changes towards normal, except Cx43 lateralization. Opening of Cx43 hemichannels was blocked by apocynin treatment and by acute hemichannel blockade with carbenoxolone. NADPH oxidase inhibition also prevented the occurrence of apoptosis in mdx hearts and reversed the ventricular remodeling. These results show that NADPH oxidase activity in DMD is associated with S-nitrosylation and opening of Cx43 hemichannels. These changes lead to apoptosis and cardiac dysfunction and were prevented by NADPH oxidase inhibition.

Indexed as

MyocardiumAcetophenonesAnimalsConnexin 43Enzyme InhibitorsMaleMiceMice, Inbred mdxMuscular Dystrophy, DuchenneNADPH OxidasesNitrosative StressOxidative StressAcetophenonesacetovanilloneConnexin 43Enzyme InhibitorsGJA1 protein, mouseNADPH OxidasesDuchenneheartNADPH oxidaseNOX2S-nitrosylation

Identifiers

PMID32751416
PMCPMC7432655
OpenAlexW3045885411

What OpenQuestion holds

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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.