Evidence map›Paper›PMID 27730652›Full record

ArticleThe Journal of physiology2016

Role of dynamin-related protein 1-mediated mitochondrial fission in resistance of mouse C2C12 myoblasts to heat injury.

Tianzheng Yu, Patricia Deuster, Yifan Chen

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of physiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
1.6field-weighted citation impact, top 16% 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

19 citing papers in PubMed, 32 citations in OpenAlex.

  1. Article
  2. Tau protein as a regulator of mitochondrial function and dynamics.Proceedings of the National Academy of Sciences of the United States of America · 2026
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  16. Mitochondrial division inhibitor 1 (mdivi-1) increases oxidative capacity and contractile stress generated by engineered skeletal muscle.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2020
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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

3 authors at 1 institution in 1 country.

Tianzheng YuDepartment of Military and Emergency Medicine, Uniformed Services University of the Health Sciences, Bethesda, MD, 20814, USA.
Patricia DeusterDepartment of Military and Emergency Medicine, Uniformed Services University of the Health Sciences, Bethesda, MD, 20814, USA.
Yifan ChenDepartment of Military and Emergency Medicine, Uniformed Services University of the Health Sciences, Bethesda, MD, 20814, USA.ORCID 0000-0003-1388-9200
Uniformed Services University of the Health Sciences · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

key pointsUnderstanding how skeletal muscles respond to high temperatures may help develop strategies for improving exercise tolerance and preventing heat injury. Mitochondria regulate cell survival by constantly changing their morphology through fusion and fission in response to environmental stimuli. Little is known about the involvement of mitochondrial dynamics in tolerance of skeletal muscle against heat stress. Mild heat acclimation and moderate heat shock appear to have different effects on the mitochondrial morphology and fission protein Drp1 in skeletal muscle cells. Mitochondrial integrity plays a key role in cell survival under heat stress. ABSTRACT: The regulation of mitochondrial morphology is closely coupled to cell survival during stress. We examined changes in the mitochondrial morphology of mouse C2C12 skeletal muscle cells in response to heat acclimation and heat shock exposure. Acclimated cells showed a greater survival rate during heat shock exposure than non-acclimated cells, and were characterized by long interconnected mitochondria and reduced expression of dynamin-related protein 1 (Drp1) for their mitochondrial fractions. Exposure of C2C12 muscle cells to heat shock led to apoptotic death featuring activation of caspase 3/7, release of cytochrome c and loss of cell membrane integrity. Heat shock also caused excessive mitochondrial fragmentation, loss of mitochondrial membrane potential and production of reactive oxygen species in C2C12 cells. Western blot and immunofluorescence image analysis revealed translocation of Drp1 to mitochondria from the cytosol in C2C12 cells exposed to heat shock. Mitochondrial division inhibitor 1 or Drp1 gene silencer reduced mitochondrial fragmentation and increased cell viability during exposure to heat shock. These results suggest that Drp1-dependent mitochondrial fission may regulate susceptibility to heat-induced apoptosis in muscle cells and that Drp1 may serve as a target for the prevention of heat-related injury.

Indexed as

AnimalsApoptosisCell LineCell SurvivalDynaminsHeat-Shock ResponseHot TemperatureMaleMembrane Potential, MitochondrialMice, Inbred C57BLMicroscopy, Electron, TransmissionMitochondrial DynamicsMitochondria, MuscleMuscle, SkeletalMyoblastsReactive Oxygen SpeciesDnm1l protein, mouseDynaminsReactive Oxygen Speciesapoptosisheat acclimationheat stressmitochondrial division inhibitor-1mitochondrial dynamicsreactive oxygen speciesskeletal muscle

Identifiers

PMID27730652
PMCPMC5157065
OpenAlexW2529932479

What OpenQuestion holds

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Registered trials

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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.