Evidence map›Paper›PMID 31273946›Full record

ReviewJournal of cellular and molecular medicine2019

Muscle wasting: A review of exercise, classical and non-classical RAS axes.

Mark A Winslow, Stephanie E Hall

Open access · goldAbstract readReview
In one paragraph

Review in Journal of cellular and molecular medicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
1.0field-weighted citation impact, top 23% 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

10 citing papers in PubMed, 13 citations in OpenAlex.

  1. Review
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  8. ACE2, angiotensin 1-7 and skeletal muscle: review in the era of COVID-19.Clinical science (London, England : 1979) · 2020
    Review
  9. Review
  10. Muscle wasting: A review of exercise, classical and non-classical RAS axes.Journal of cellular and molecular medicine · 2019
    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

2 authors at 1 institution in 1 country.

Mark A WinslowDepartment of Kinesiology, Boise State University, Boise, Idaho.ORCID 0000-0002-2950-8399
Stephanie E HallDepartment of Kinesiology, Boise State University, Boise, Idaho.
Boise State University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

This review identifies how the classical/non-classical renin-angiotensin system (RAS) and exercise influence muscle wasting. The classical RAS axis enhances muscle loss through the interaction with NADPH oxidase (NOX), ubiquitin proteasome system (UPS), protein synthesis and fibrosis pathways. The mainstream hypothesis identifies reactive oxygen species (ROS) as the key pathway in muscle, this review recognizes alternative pathways that lead to an increase in muscle wasting through the classical RAS axis. In addition, pathways in which the non-classical RAS axis and exercise inhibit the classical RAS axis are also explored. The non-classical RAS axis and exercise have a significant negative impact on ROS production and protein synthesis. The non-classical RAS axis has been identified in this review to directly affect protein synthesis pathways not by altering the pre-existing intracellular ROS level, further supporting the idea that muscle wasting caused by the classical RAS system is not entirely due to ROS production. Exercise has been identified to modify the RAS axes making it a therapeutic option.

Indexed as

Angiotensin IAngiotensin IIApoptosisExerciseFibrosisHumansMitochondriaMuscle, SkeletalMuscular AtrophyNADPH OxidasesPeptide FragmentsProtein BiosynthesisReactive Oxygen SpeciesRenin-Angiotensin SystemUbiquitin-Protein LigasesAngiotensin Iangiotensin I (1-7)Angiotensin IINADPH OxidasesPeptide FragmentsReactive Oxygen SpeciesUbiquitin-Protein LigasesAngiotensin 1-7Angiotensin IIexercisefibrosisprotein synthesisROSUPS

Identifiers

PMID31273946
PMCPMC6714228
OpenAlexW2956065556

What OpenQuestion holds

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LicenceCC BY
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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.