Evidence map›Paper›PMID 31526891›Full record

ArticleMitochondrion2019

Fis1 deficiencies differentially affect mitochondrial quality in skeletal muscle.

Zhe Zhang, Danielle A Sliter, Christopher K E Bleck, Shuzhe Ding

Open access · greenAbstract read
In one paragraph

Article in Mitochondrion, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
1.5field-weighted citation impact, top 18% 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

25 citing papers in PubMed, 39 citations in OpenAlex.

  1. Article
  2. Dying oligodendrocytes persist without mitochondria.bioRxiv : the preprint server for biology · 2026
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  13. Article
  14. Article
  15. Article
  16. Article
  17. Review
  18. The Role of Mitochondrial Dynamin in Stroke.Oxidative medicine and cellular longevity · 2022
    Review
  19. Article
  20. Article
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 2 countries.

Zhe ZhangKey Laboratory of Adolescent Health Assessment and Exercise Intervention of Ministry of Education, East China Normal University, Shanghai 200241, China; Biochemistry Section, Surgical Neurology Branch, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD 20892, USA; School of Physical Education and Health care, East China Normal University, Shanghai 200241, China. Electronic address: zhangzhe@tyxx.ecnu.edu.cn.
Danielle A SliterBiochemistry Section, Surgical Neurology Branch, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD 20892, USA.
Christopher K E BleckElectron Microscopy Core Facility, National Heart, Lung and Blood Institute (NHLBI), National Institutes of Health, Bethesda, MD 20892, USA.
Shuzhe DingKey Laboratory of Adolescent Health Assessment and Exercise Intervention of Ministry of Education, East China Normal University, Shanghai 200241, China; School of Physical Education and Health care, East China Normal University, Shanghai 200241, China. Electronic address: szding@tyxx.ecnu.edu.cn.
National Institutes of Health · USEast China Normal University · CN

Funding

Intramural NIH HHS Z99 HL999999
6 · The paper itself

Abstract

Mitochondrial dynamics and mitophagy are important aspects of mitochondrial quality control, and are linked to neurodegenerative diseases and muscular diseases. Fis1, a protein on the mitochondrial outer membrane, is thought to mediate mitochondrial fission. However, Fis1 null worms and mammalian cells only display mild fission defects but show aberrant mitophagy. To assess Fis1 function in vivo, we generated conditional knock-out Fis1 mice to allow for specific Fis1 deletion in adult skeletal muscle. In the absence of Fis1 in Type I muscle, mitochondrial hyperfusion, respiratory chain deficiency, and increased mitophagy were found. Moreover, abnormal mitophagy was aggravated by endurance exhaustive exercise stress (EEE), suggesting that Fis1 is involved in maintaining normal mitophagy in mitochondria-rich Type I muscle during exercise. Additionally, Fis1 loss induced delayed onset muscle ultrastructure change (DOMUC) in Type I muscle and strong inflammation in response to acute exhaustive exercise (EE). Thus, we identify a role for Fis1 in maintaining normal mitochondrial structure and function at rest and under exercise stress.

Indexed as

MitophagyPhysical Conditioning, AnimalStress, PhysiologicalAnimalsMiceMice, KnockoutMitochondrial ProteinsMitochondria, MuscleMuscle, SkeletalFIS1 protein, mouseMitochondrial ProteinsExhaustive exerciseFis1Inflammation responseMitochondrial dynamicsMitophagy

Identifiers

PMID31526891
PMCPMC7097820
OpenAlexW2972555119

What OpenQuestion holds

Textmetadata
LicenceTDM
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.