Evidence map›Paper›PMID 34685566›Full record

ArticleCells2021

Mitochondrial Permeability Transition Causes Mitochondrial Reactive Oxygen Species- and Caspase 3-Dependent Atrophy of Single Adult Mouse Skeletal Muscle Fibers.

Sarah K Skinner, Angelo Solania, Dennis W Wolan, Michael S Cohen, Terence E Ryan, Russell T Hepple

Open access · goldAbstract read
In one paragraph

Article in Cells, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
1.1field-weighted citation impact, top 24% 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

11 citing papers in PubMed, 21 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
  4. Redox regulation of UPR signalling and mitochondrial ER contact sites.Cellular and molecular life sciences : CMLS · 2024
    Review
  5. Article
  6. Mitochondrial dysfunction: roles in skeletal muscle atrophy.Journal of translational medicine · 2023
    Review
  7. Review
  8. Mitochondrial Permeability Transition in Stem Cells, Development, and Disease.Advances in experimental medicine and biology · 2023
    Review
  9. Article
  10. Review
  11. 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

6 authors at 3 institutions in 1 country.

Sarah K SkinnerDepartment of Physical Therapy, University of Florida, Gainesville, FL 32610, USA.ORCID 0000-0002-3049-2216
Angelo SolaniaDepartments of Molecular Medicine and Integrative Structural and Computational Biology, Scripps Research, La Jolla, San Diego, CA 92037, USA.
Dennis W WolanDepartments of Molecular Medicine and Integrative Structural and Computational Biology, Scripps Research, La Jolla, San Diego, CA 92037, USA.
Michael S CohenDepartment of Chemical Physiology and Biochemistry, Oregon Health and Science University, Portland, OR 97239, USA.ORCID 0000-0002-7636-4156
Terence E RyanDepartment of Applied Physiology and Kinesiology, University of Florida, Gainesville, FL 32610, USA.ORCID 0000-0003-0780-029X
Russell T HeppleDepartment of Physical Therapy, University of Florida, Gainesville, FL 32610, USA.
University of Florida · USScripps Institution of Oceanography · USOregon Health & Science University · US

Funding

Training In Rehabilitation and Neuromuscular PlasticityT32HD043730 · NICHD · UNIVERSITY OF FLORIDA · PI DAVID D FULLER · 2003 to 2026
$5.3M
National Institute of Child Health and Human Development T32HD043730University of Florida Opportunity Seed Fund
6 · The paper itself

Abstract

Elevated mitochondrial reactive oxygen species (mROS) and an increase in caspase-3 activity are established mechanisms that lead to skeletal muscle atrophy via the upregulation of protein degradation pathways. However, the mechanisms upstream of an increase in mROS and caspase-3 activity in conditions of muscle atrophy have not been identified. Based upon knowledge that an event known as mitochondrial permeability transition (MPT) causes an increase in mROS emission and the activation of caspase-3 via mitochondrial release of cytochrome c, as well as the circumstantial evidence for MPT in some muscle atrophy conditions, we tested MPT as a mechanism of atrophy. Briefly, treating cultured single mouse flexor digitorum brevis (FDB) fibers from adult mice with a chemical inducer of MPT (Bz423) for 24 h caused an increase in mROS and caspase-3 activity that was accompanied by a reduction in muscle fiber diameter that was able to be prevented by inhibitors of MPT, mROS, or caspase-3 (

Indexed as

AnimalsCaspase 3Disease Models, AnimalMaleMiceMitochondrial Transmembrane Permeability-Driven NecrosisMuscle Fibers, SkeletalReactive Oxygen SpeciesCasp3 protein, mouseCaspase 3Reactive Oxygen Speciescaspase-3mitochondrial permeability transition poreROSskeletal muscle atrophy

Identifiers

PMID34685566
PMCPMC8534155
OpenAlexW3204439450

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.