Evidence map›Paper›PMID 26851244›Full record

ArticleDisease models & mechanisms2016

Angiotensin-(1-7) attenuates disuse skeletal muscle atrophy in mice via its receptor, Mas.

María Gabriela Morales, Johanna Abrigo, María José Acuña, Robson A Santos, Michael Bader, Enrique Brandan, Felipe Simon, Hugo Olguin, Daniel Cabrera, Claudio Cabello-Verrugio

Open access · goldAbstract read
In one paragraph

Article in Disease models & mechanisms, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.

0numbers the graph read from it
0cells of the map it votes in
47citing papers in PubMed
5.0field-weighted citation impact, top 4% 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

47 citing papers in PubMed, 83 citations in OpenAlex.

  1. Article
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  7. Angiotensin-(1-7) improves skeletal muscle regeneration.European journal of translational myology · 2023
    Article
  8. Effect of physical activity on long COVID fatigue: an unsolved enigma.European journal of translational myology · 2023
    Article
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  10. Review
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  20. The Critical Role of Oxidative Stress in Sarcopenic Obesity.Oxidative medicine and cellular longevity · 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

10 authors at 5 institutions in 3 countries.

María Gabriela MoralesLaboratory of Biology and Molecular Physiopathology, Department of Biological Sciences, Faculty of Biological Sciences & Faculty of Medicine, Universidad Andrés Bello, Santiago 8370146, Chile Millennium Institute on Immunology and Immunotherapy, Santiago 8370146, Chile.
Johanna AbrigoLaboratory of Biology and Molecular Physiopathology, Department of Biological Sciences, Faculty of Biological Sciences & Faculty of Medicine, Universidad Andrés Bello, Santiago 8370146, Chile Millennium Institute on Immunology and Immunotherapy, Santiago 8370146, Chile.
María José AcuñaCenter for Cell Regulation and Pathology (CRCP), Center for Regeneration and Aging (CARE), Laboratory of Cell Differentiation and Pathology, Department of Cell and Molecular Biology, Faculty of Biological Sciences, P. Universidad Católica de Chile, Santiago 8331150, Chile.
Robson A SantosNational Institute in Science and Technology in Nanobiopharmaceutics, Department of Physiology and Biophysics, Federal University of Minas Gerais (UFMG), Belo Horizonte 31270-901, Brazil.
Michael BaderMax-Delbrück-Center for Molecular Medicine, Berlin-Buch 13125, Germany National Institute in Science and Technology in Nanobiopharmaceutics, Belo Horizonte 31270-901, Brazil.
Enrique BrandanCenter for Cell Regulation and Pathology (CRCP), Center for Regeneration and Aging (CARE), Laboratory of Cell Differentiation and Pathology, Department of Cell and Molecular Biology, Faculty of Biological Sciences, P. Universidad Católica de Chile, Santiago 8331150, Chile.
Felipe SimonLaboratory of Integrative Physiopathology, Department of Biological Sciences, Faculty of Biological Sciences & Faculty of Medicine, Universidad Andrés Bello, Santiago 8370146, Chile Millennium Institute on Immunology and Immunotherapy, Santiago 8370146, Chile.
Hugo OlguinLaboratory of Tissue Repair and Adult Stem Cells, Department of Cell and Molecular Biology, Faculty of Biological Sciences, P. Universidad Católica de Chile, Santiago 8331150, Chile.
Daniel CabreraDepartamento de Ciencias Químicas y Biológicas, Facultad de Salud, Universidad Bernardo O Higgins, Santiago 8370993, Chile Departamento de Gastroenterología, Facultad de Medicina, Pontificia Universidad Católica de Chile, Santiago 8330024, Chile.
Claudio Cabello-VerrugioLaboratory of Biology and Molecular Physiopathology, Department of Biological Sciences, Faculty of Biological Sciences & Faculty of Medicine, Universidad Andrés Bello, Santiago 8370146, Chile Millennium Institute on Immunology and Immunotherapy, Santiago 8370146, Chile claudio.cabello@unab.cl.
Millennium Institute on Immunology and Immunotherapy · CLPontificia Universidad Católica de Chile · CLMax Delbrück Center · DEUniversidad Bernardo O'Higgins · CLUniversidade Federal de Minas Gerais · BR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Immobilization is a form of disuse characterized by a loss of strength and muscle mass. Among the main features are decreased IGF-1/Akt signalling and increased ubiquitin-proteasome pathway signalling, which induce greater myosin heavy chain degradation. Activation of the classical renin-angiotensin system (RAS) causes deleterious effects in skeletal muscle, including muscle wasting. In contrast, angiotensin-(1-7) [Ang-(1-7)], a peptide of the non-classical RAS, produces beneficial effects in skeletal muscle. However, the role of Ang-(1-7) in skeletal muscle disuse atrophy and independent of classical RAS activation has not been evaluated. Therefore, we assessed the functions of Ang-(1-7) and the Mas receptor in disuse muscle atrophyin vivousing unilateral cast immobilization of the hind limb in male, 12-week-old wild-type (WT) and Mas-knockout (Mas KO) mice for 1 and 14 days. Additionally, we evaluated the participation of IGF-1/IGFR-1/Akt signalling and ubiquitin-proteasome pathway expression on the effects of Ang-(1-7) immobilization-induced muscle atrophy. Our results found that Ang-(1-7) prevented decreased muscle strength and reduced myofiber diameter, myosin heavy chain levels, and the induction of atrogin-1 and MuRF-1 expressions, all of which normally occur during immobilization. Analyses indicated that Ang-(1-7) increases IGF-1/IGFR-1/Akt pathway signalling through IGFR-1 and Akt phosphorylation, and the concomitant activation of two downstream targets of Akt, p70S6K and FoxO3. These anti-atrophic effects of Ang-(1-7) were not observed in Mas KO mice, indicating crucial participation of the Mas receptor. This report is the first to propose anti-atrophic effects of Ang-(1-7) via the Mas receptor and the participation of the IGF-1/IGFR-1/Akt/p70S6K/FoxO3 mechanism in disuse skeletal muscle atrophy.

Indexed as

Angiotensin IAnimalsInsulin-Like Growth Factor IIsometric ContractionMaleMiceMice, Inbred C57BLMuscle Fibers, SkeletalMuscle ProteinsMuscle StrengthMuscular AtrophyMuscular Disorders, AtrophicMyosin Heavy ChainsPeptide FragmentsProto-Oncogene MasProto-Oncogene ProteinsAngiotensin Iangiotensin I (1-7)Fbxo32 protein, mouseInsulin-Like Growth Factor IMuscle ProteinsMyosin Heavy ChainsPeptide FragmentsProto-Oncogene MasProto-Oncogene ProteinsProto-Oncogene Proteins c-aktReceptor, IGF Type 1Receptors, G-Protein-CoupledSKP Cullin F-Box Protein LigasesTrim63 protein, mouseTripartite Motif ProteinsUbiquitin-Protein LigasesAngiotensin-(1-7)AtrophyDisuseMas receptorSkeletal muscle

Identifiers

PMID26851244
PMCPMC4852504
OpenAlexW2312328558

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.