Evidence map›Paper›PMID 30833900›Full record

ReviewFrontiers in physiology2019

The Skeletal Muscle as an Active Player Against Cancer Cachexia.

Fabio Penna, Riccardo Ballarò, Marc Beltrà, Serena De Lucia, Lorena García Castillo, Paola Costelli

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in physiology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed, 1 pooled it
4.0field-weighted citation impact, top 5% 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

39 citing papers in PubMed, 1 synthesis or guideline pooled it, 68 citations in OpenAlex.

  1. Pooled it
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  14. Muscle and Bone Defects in Metastatic Disease.Current osteoporosis reports · 2022
    Review
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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 1 institution in 1 country.

Fabio PennaDepartment of Clinical and Biological Sciences, Interuniversity Institute of Myology, University of Turin, Turin, Italy.
Riccardo BallaròDepartment of Clinical and Biological Sciences, Interuniversity Institute of Myology, University of Turin, Turin, Italy.
Marc BeltràDepartment of Clinical and Biological Sciences, Interuniversity Institute of Myology, University of Turin, Turin, Italy.
Serena De LuciaDepartment of Clinical and Biological Sciences, Interuniversity Institute of Myology, University of Turin, Turin, Italy.
Lorena García CastilloDepartment of Clinical and Biological Sciences, Interuniversity Institute of Myology, University of Turin, Turin, Italy.
Paola CostelliDepartment of Clinical and Biological Sciences, Interuniversity Institute of Myology, University of Turin, Turin, Italy.
University of Turin · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The management of cancer patients is frequently complicated by the occurrence of cachexia. This is a complex syndrome that markedly impacts on quality of life as well as on tolerance and response to anticancer treatments. Loss of body weight, wasting of both adipose tissue and skeletal muscle and reduced survival rates are among the main features of cachexia. Skeletal muscle wasting has been shown to depend, mainly at least, on the induction of protein degradation rates above physiological levels. Such hypercatabolic pattern is driven by overactivation of different intracellular proteolytic systems, among which those dependent on ubiquitin-proteasome and autophagy. Selective rather than bulk degradation of altered proteins and organelles was also proposed to occur. Within the picture described above, the muscle is frequently considered a sort of by-stander tissue where external stimuli, directly or indirectly, can poise protein metabolism toward a catabolic setting. By contrast, several observations suggest that the muscle reacts to the wasting drive imposed by cancer growth by activating different compensatory strategies that include anabolic capacity, the activation of autophagy and myogenesis. Even if muscle response is eventually ill-fated, its occurrence supports the idea that in the presence of appropriate treatments the development of cancer-induced wasting might not be an ineluctable event in tumor hosts.

Indexed as

adaptive responseenergy metabolismmuscle wastingmyogenesisoxidative stressprotein turnover

Identifiers

PMID30833900
PMCPMC6387914
OpenAlexW2910535306

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.