Evidence map›Paper›PMID 32050585›Full record

ArticleInternational journal of molecular sciences2020

Angiotensin (1-7) Decreases Myostatin-Induced NF-κB Signaling and Skeletal Muscle Atrophy.

Javier Aravena, Johanna Abrigo, Francisco Gonzalez, Francisco Aguirre, Andrea Gonzalez, Felipe Simon, Claudio Cabello-Verrugio

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 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
2.2field-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

23 citing papers in PubMed, 35 citations in OpenAlex.

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  8. Angiotensin-(1-7) improves skeletal muscle regeneration.European journal of translational myology · 2023
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  20. Regulation of Myostatin on the Growth and Development of Skeletal Muscle.Frontiers in cell and developmental biology · 2021
    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

7 authors at 2 institutions in 1 country.

Javier AravenaLaboratory of Muscle Pathology, Fragility and Aging, Department of Biological Sciences, Faculty of Life Sciences, Universidad Andres Bello, 8370146 Santiago, Chile.
Johanna AbrigoLaboratory of Muscle Pathology, Fragility and Aging, Department of Biological Sciences, Faculty of Life Sciences, Universidad Andres Bello, 8370146 Santiago, Chile.
Francisco GonzalezLaboratory of Muscle Pathology, Fragility and Aging, Department of Biological Sciences, Faculty of Life Sciences, Universidad Andres Bello, 8370146 Santiago, Chile.
Francisco AguirreLaboratory of Muscle Pathology, Fragility and Aging, Department of Biological Sciences, Faculty of Life Sciences, Universidad Andres Bello, 8370146 Santiago, Chile.
Andrea GonzalezLaboratory of Muscle Pathology, Fragility and Aging, Department of Biological Sciences, Faculty of Life Sciences, Universidad Andres Bello, 8370146 Santiago, Chile.
Felipe SimonMillennium Institute on Immunology and Immunotherapy, 8370146 Santiago, Chile.
Claudio Cabello-VerrugioLaboratory of Muscle Pathology, Fragility and Aging, Department of Biological Sciences, Faculty of Life Sciences, Universidad Andres Bello, 8370146 Santiago, Chile.
Universidad de Santiago de Chile · CLUniversidad Andrés Bello · CL

Funding

BASAL Grant CEDENNA FB0807Millennium Institute on Immunology and Immunotherapy P09-016-FNational Fund for Science and Technological Development 1161646; 1161288Programa de Cooperación Científica ECOS-CONICYT C16S02
6 · The paper itself

Abstract

Myostatin is a myokine that regulates muscle function and mass, producing muscle atrophy. Myostatin induces the degradation of myofibrillar proteins, such as myosin heavy chain or troponin. The main pathway that mediates protein degradation during muscle atrophy is the ubiquitin proteasome system, by increasing the expression of atrogin-1 and MuRF-1. In addition, myostatin activates the NF-κB signaling pathway. Renin-angiotensin system (RAS) also regulates muscle mass. Angiotensin (1-7) (Ang-(1-7)) has anti-atrophic properties in skeletal muscle. In this paper, we evaluated the effect of Ang-(1-7) on muscle atrophy and signaling induced by myostatin. The results show that Ang-(1-7) prevented the decrease of the myotube diameter and myofibrillar protein levels induced by myostatin. Ang-(1-7) also abolished the increase of myostatin-induced reactive oxygen species production, atrogin-1, MuRF-1, and TNF-α gene expressions and NF-κB signaling activation. Ang-(1-7) inhibited the activity mediated by myostatin through Mas receptor, as is demonstrated by the loss of all Ang-(1-7)-induced effects when the Mas receptor antagonist A779 was used. Our results show that the effects of Ang-(1-7) on the myostatin-dependent muscle atrophy and signaling are blocked by MK-2206, an inhibitor of Akt/PKB. Together, these data indicate that Ang-(1-7) inhibited muscle atrophy and signaling induced by myostatin through a mechanism dependent on Mas receptor and Akt/PKB.

Indexed as

Signal TransductionAngiotensin IAnimalsCell LineMiceMuscle Fibers, SkeletalMuscle ProteinsMyostatinNF-kappa BPeptide FragmentsReactive Oxygen SpeciesSKP Cullin F-Box Protein LigasesTripartite Motif ProteinsTumor Necrosis Factor-alphaUbiquitin-Protein LigasesAngiotensin Iangiotensin I (1-7)Fbxo32 protein, mouseMuscle ProteinsMyostatinNF-kappa BPeptide FragmentsReactive Oxygen SpeciesSKP Cullin F-Box Protein LigasesTrim63 protein, mouseTripartite Motif ProteinsTumor Necrosis Factor-alphaUbiquitin-Protein LigasesAkt/PKBAngiotensin-(1-7)muscle atrophyNF-κB signalingRAS

Identifiers

PMID32050585
PMCPMC7037856
OpenAlexW3004783555

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.