Evidence map›Paper›PMID 25208653›Full record

ArticleHistochemistry and cell biology2015

Expression of the Mas receptor is upregulated in skeletal muscle wasting.

María Gabriela Morales, Johanna Abrigo, Carla Meneses, Franco Cisternas, Felipe Simon, Claudio Cabello-Verrugio

Abstract read
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In one paragraph

Article in Histochemistry and cell biology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
1.9field-weighted citation impact, top 15% 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

21 citing papers in PubMed, 36 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. CoQ10 augments candesartan protective effect against tourniquet-induced hind limb ischemia-reperfusion: Involvement of non-classical RAS and ROS pathways.Saudi pharmaceutical journal : SPJ : the official publication of the Saudi Pharmaceutical Society · 2021
    Article
  7. Article
  8. ACE2, angiotensin 1-7 and skeletal muscle: review in the era of COVID-19.Clinical science (London, England : 1979) · 2020
    Review
  9. Article
  10. Article
  11. Article
  12. Muscle wasting: A review of exercise, classical and non-classical RAS axes.Journal of cellular and molecular medicine · 2019
    Review
  13. The Renin-Angiotensin System and Skeletal Muscle.Exercise and sport sciences reviews · 2018
    Review
  14. Review
  15. Review
  16. Article
  17. Effects of ACE2 deficiency on physical performance and physiological adaptations of cardiac and skeletal muscle to exercise.Hypertension research : official journal of the Japanese Society of Hypertension · 2016
    Article
  18. Article
  19. Review
  20. 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

6 authors at 2 institutions in 1 country.

María Gabriela MoralesLaboratorio de Biología y Fisiopatología Molecular, Departamento de Ciencias Biológicas, Facultad de Ciencias Biológicas & Facultad de Medicina, Universidad Andres Bello, Avenida República 239, 8370146, Santiago, Chile.
Johanna Abrigo
Carla Meneses
Franco Cisternas
Felipe Simon
Claudio Cabello-Verrugio
Universidad Andrés Bello · CLMillennium Institute on Immunology and Immunotherapy · CL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Skeletal muscle atrophy during sepsis, immobilization, and chronic diseases is characterized by an increase in expression and activity of the muscle-specific ubiquitin 3 ligases atrogin-1 and MuRF-1. The classical renin-angiotensin system (RAS), by high level of circulating angiotensin II (AngII) is directly involved in skeletal muscle wasting associated with cardiac and renal failure. Ang (1-7), a peptide belonging to the non-classical RAS system, produces effects that are opposite to AngII. The actions of Ang (1-7) are mediated by its binding and signalling through the Mas receptor. Our purpose is to assess the effects of atrophic stimuli AngII, lipopolysaccharide (LPS), and immobilization on the expression of the Mas receptor in skeletal muscle. For that we used gastrocnemius and tibialis anterior muscles of C57BL10 mice treated with AngII, LPS or subjected to unilateral hindlimb immobilization by casting. In addition, we used C2C12 myotubes incubated with AngII or LPS. We evaluated Mas expression by quantitative real-time PCR, Western blot immunohistochemical analysis. Skeletal muscle atrophy was corroborated by the expression of atrogin-1 and MuRF-1 and the fibre diameter. Our results show that Mas receptor expression was increased by AngII or LPS in vitro and in vivo, and upregulated by immobilization. The increase of the Mas expression was concomitantly with the upregulation of atrogin-1 and MuRF-1 and the reduction of the fibre diameter. These results from studies in vitro and in vivo demonstrate for the first time that the Mas receptor is increased under atrophic stimulus and suggest that the non-classical RAS system could have an important role in muscle wasting.

Indexed as

Up-RegulationAngiotensin IIAnimalsCells, CulturedImmunoblottingLipopolysaccharidesMaleMiceMice, Inbred C57BLMuscle, SkeletalMuscular AtrophyPolymerase Chain ReactionProtein BindingReceptors, G-Protein-CoupledAngiotensin IILipopolysaccharidesReceptors, G-Protein-Coupled

Identifiers

PMID25208653
OpenAlexW2000853233

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

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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.