Evidence map›Paper›PMID 29615929›Full record

ReviewFrontiers in physiology2018

Muscle Atrophy Induced by Mechanical Unloading: Mechanisms and Potential Countermeasures.

Yunfang Gao, Yasir Arfat, Huiping Wang, Nandu Goswami

Open access · goldAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Frontiers in physiology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 149 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
149citing papers in PubMed, 4 pooled it
10.2field-weighted citation impact, top 1% 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

149 citing papers in PubMed, 4 syntheses or guidelines pooled it, 266 citations in OpenAlex.

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  10. Tailored postoperative bracing strategies following three distinct lumbar endoscopic discectomy: a propensity score-matched analysis.European spine journal : official publication of the European Spine Society, the European Spinal Deformity Society, and the European Section of the Cervical Spine Research Society · 2026
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89 more citing papers are in PubMed but not listed here.

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

4 authors at 3 institutions in 2 countries.

Yunfang GaoKey Laboratory of Resource Biology and Biotechnology in Western China, College of Life Sciences, Ministry of Education, Northwest University, Xi'an, China.
Yasir ArfatKey Laboratory of Resource Biology and Biotechnology in Western China, College of Life Sciences, Ministry of Education, Northwest University, Xi'an, China.
Huiping WangKey Laboratory of Resource Biology and Biotechnology in Western China, College of Life Sciences, Ministry of Education, Northwest University, Xi'an, China.
Nandu GoswamiPhysiology Unit, Otto Loewi Center of Research for Vascular Biology, Immunity and Inflammation, Medical University of Graz, Graz, Austria.
Ministry of Education of the People's Republic of China · CNMedical University of Graz · ATNorthwest University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Prolonged periods of skeletal muscle inactivity or mechanical unloading (bed rest, hindlimb unloading, immobilization, spaceflight and reduced step) can result in a significant loss of musculoskeletal mass, size and strength which ultimately lead to muscle atrophy. With advancement in understanding of the molecular and cellular mechanisms involved in disuse skeletal muscle atrophy, several different signaling pathways have been studied to understand their regulatory role in this process. However, substantial gaps exist in our understanding of the regulatory mechanisms involved, as well as their functional significance. This review aims to update the current state of knowledge and the underlying cellular mechanisms related to skeletal muscle loss during a variety of unloading conditions, both in humans and animals. Recent advancements in understanding of cellular and molecular mechanisms, including IGF1-Akt-mTOR, MuRF1/MAFbx, FOXO, and potential triggers of disuse atrophy, such as calcium overload and ROS overproduction, as well as their role in skeletal muscle protein adaptation to disuse is emphasized. We have also elaborated potential therapeutic countermeasures that have shown promising results in preventing and restoring disuse-induced muscle loss. Finally, identified are the key challenges in this field as well as some future prospectives.

Indexed as

disuse muscle atrophymechanical unloadingmolecular and cellular pathwaysprotein degradationprotein synthesistherapeutic countermeasures

Identifiers

PMID29615929
PMCPMC5869217
OpenAlexW2790623308

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.