Evidence map›Paper›PMID 30452895›Full record

ReviewArchives of biochemistry and biophysics2019

Mitochondrial dysfunction induces muscle atrophy during prolonged inactivity: A review of the causes and effects.

Hayden Hyatt, Rafael Deminice, Toshinori Yoshihara, Scott K Powers

Registry-linked trialAbstract readReview
In one paragraph

Review in Archives of biochemistry and biophysics, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT07690150 (A Novel Angle), which is not on this map. Cited by 124 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
124citing papers in PubMed, 2 pooled it
5.8field-weighted citation impact, top 3% 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.

NCT07690150 nanot yet recruitingnot on this mapstarted 2026, after this paper: background citation

A Novel Angle: Manipulating Knee Position to Understand Muscle Deterioration During Leg Immobilization

TypeinterventionalSponsorWageningen UniversityRan2026 to 2028Enrolled30ConditionsMuscle Atrophy, Disuse Atrophy, ImmobilizationArmsKnee immobilization brace (0°) for 5 days, Knee immobilization brace (60°) for 5 days
3 · Its place in the literature

Who cites it

124 citing papers in PubMed, 2 syntheses or guidelines pooled it, 205 citations in OpenAlex.

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  17. The role of sestrin2 in skeletal muscle regeneration after injury.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2026
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64 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 2 institutions in 3 countries.

Hayden HyattDepartment of Applied Physiology and Kinesiology, University of Florida, Gainesville, FL, USA. Electronic address: haydenhyatt@ufl.edu.
Rafael DeminiceDepartment of Applied Physiology and Kinesiology, University of Florida, Gainesville, FL, USA; Department of Physical Education, University of Estadual of Londrina, Londrina, Brazil.
Toshinori YoshiharaDepartment of Applied Physiology and Kinesiology, University of Florida, Gainesville, FL, USA; Department of Exercise Physiology, Juntendo University, Tokyo, Japan.
Scott K PowersDepartment of Applied Physiology and Kinesiology, University of Florida, Gainesville, FL, USA.
University of Florida · USUniversidade Estadual de Londrina · BR

Funding

Mechanisms of exercise protection in ventilator-induced diaphragm dysfunctionR01AR064189 · NIAMS · UNIVERSITY OF FLORIDA · PI POWERS, SCOTT K. · 2013 to 2017
$2.2M
NIAMS NIH HHS R01 AR064189
6 · The paper itself

Abstract

Prolonged skeletal muscle inactivity (e.g. limb immobilization, bed rest, mechanical ventilation, spinal cord injury, etc.) results in muscle atrophy that manifests into a decreased quality of life and in select patient populations, a higher risk of morbidity and mortality. Thus, understanding the processes that contribute to muscle atrophy during prolonged periods of muscle disuse is an important area of research. In this regard, mitochondrial dysfunction has been directly linked to the muscle wasting that occurs during extended periods of skeletal muscle inactivity. While the concept that mitochondrial dysfunction contributes to disuse muscle atrophy has been contemplated for nearly 50 years, the mechanisms connecting mitochondrial signaling events to skeletal muscle atrophy remained largely unexplained until recently. Indeed, emerging evidence reveals that mitochondrial dysfunction and the associated mitochondrial signaling events are a requirement for several forms of inactivity-induced skeletal muscle atrophy. Specifically, inactivity-induced alterations in skeletal muscle mitochondria phenotype and increased ROS emission, impaired Ca

Indexed as

Sedentary BehaviorAnimalsEnergy MetabolismHomeostasisHumansMitochondria, MuscleMuscle, SkeletalMuscular AtrophyQuality of LifeReactive Oxygen SpeciesSignal TransductionReactive Oxygen SpeciesCell signalingDisuse muscle atrophyMitochondrial dysfunctionMuscle wastingProteolysisReactive oxygen species

Identifiers

PMID30452895
PMCPMC6783132
OpenAlexW2900974539

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

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.