Evidence map›Paper›PMID 22395111›Full record

ReviewAmerican journal of physiology. Endocrinology and metabolism2012

Mitochondrial signaling contributes to disuse muscle atrophy.

Scott K Powers, Michael P Wiggs, Jose A Duarte, A Murat Zergeroglu, Haydar A Demirel

Registry-linked trialOpen access · greenAbstract readReview
In one paragraph

Review in American journal of physiology. Endocrinology and metabolism, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT04368117 (STAT), which is not on this map. Cited by 129 papers.

0numbers the graph read from it
0cells of the map it votes in
129citing papers in PubMed
6.3field-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.

NCT04368117 naactive not recruitingnot on this mapstarted 2020, after this paper: background citation

STAT: Standard Therapy Plus Active Therapy to Improve Mobility, Long-Term Activity, and Quality of Life for Severely Burn Injured Patients After Skin Graft Surgery

TypeinterventionalSponsorAmerican Burn AssociationRan2020 to 2026Enrolled166ConditionsBurn Injury, Physical Injury, Thermal BurnArmsPhysical Therapy
3 · Its place in the literature

Who cites it

129 citing papers in PubMed, 246 citations in OpenAlex.

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  13. Mitochondrial Maintenance in Skeletal Muscle.Cold Spring Harbor perspectives in biology · 2025
    Review
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69 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

5 authors at 4 institutions in 3 countries.

Scott K PowersDepartment of Applied Physiology and Kinesiology, University of Florida, Gainesville, FL 32611, USA. spowers@hhp.ufl.edu
Michael P Wiggs
Jose A Duarte
A Murat Zergeroglu
Haydar A Demirel
University of Florida · USAnkara University · TRHacettepe University · TRUniversidade do Porto · PT

Funding

Mechanical Ventilation, Oxidative Stress, and Diaphragmatic AtrophyR01HL087839 · NHLBI · UNIVERSITY OF FLORIDA · PI POWERS, SCOTT K. · 2009 to 2012
$1.4M
NHLBI NIH HHS R01 HL-087839
6 · The paper itself

Abstract

It is well established that long durations of bed rest, limb immobilization, or reduced activity in respiratory muscles during mechanical ventilation results in skeletal muscle atrophy in humans and other animals. The idea that mitochondrial damage/dysfunction contributes to disuse muscle atrophy originated over 40 years ago. These early studies were largely descriptive and did not provide unequivocal evidence that mitochondria play a primary role in disuse muscle atrophy. However, recent experiments have provided direct evidence connecting mitochondrial dysfunction to muscle atrophy. Numerous studies have described changes in mitochondria shape, number, and function in skeletal muscles exposed to prolonged periods of inactivity. Furthermore, recent evidence indicates that increased mitochondrial ROS production plays a key signaling role in both immobilization-induced limb muscle atrophy and diaphragmatic atrophy occurring during prolonged mechanical ventilation. Moreover, new evidence reveals that, during denervation-induced muscle atrophy, increased mitochondrial fragmentation due to fission is a required signaling event that activates the AMPK-FoxO3 signaling axis, which induces the expression of atrophy genes, protein breakdown, and ultimately muscle atrophy. Collectively, these findings highlight the importance of future research to better understand the mitochondrial signaling mechanisms that contribute to disuse muscle atrophy and to develop novel therapeutic interventions for prevention of inactivity-induced skeletal muscle atrophy.

Indexed as

Signal TransductionAnimalsDisease Models, AnimalHumansImmobilizationMitochondrial DiseasesMitochondria, MuscleMuscle, SkeletalMuscular AtrophyMuscular Disorders, AtrophicOxidative StressProtein BiosynthesisProteolysis

Identifiers

PMID22395111
PMCPMC3404565
OpenAlexW1980638751

What OpenQuestion holds

Textmetadata
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.