Evidence map›Paper›PMID 28356270›Full record

ArticleAmerican journal of physiology. Cell physiology2017

Ulk1-mediated autophagy plays an essential role in mitochondrial remodeling and functional regeneration of skeletal muscle.

Jarrod A Call, Rebecca J Wilson, Rhianna C Laker, Mei Zhang, Mondira Kundu, Zhen Yan

Open access · bronzeAbstract read
In one paragraph

Article in American journal of physiology. Cell physiology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
47citing papers in PubMed, 1 pooled it
7.1field-weighted citation impact, top 2% 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

47 citing papers in PubMed, 1 synthesis or guideline pooled it, 79 citations in OpenAlex.

  1. Guideline
  2. Review
  3. Article
  4. Article
  5. Article
  6. Resilience of the mitochondrial reticulum in aging.American journal of physiology. Endocrinology and metabolism · 2025
    Article
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  12. Article
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  16. Article
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  19. Skeletal Muscle Regeneration in Cardiotoxin-Induced Muscle Injury Models.International journal of molecular sciences · 2022
    Review
  20. PGC-1α overexpression is not sufficient to mitigate cancer cachexia in either male or female mice.Applied physiology, nutrition, and metabolism = Physiologie appliquee, nutrition et metabolisme · 2022
    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

6 authors at 2 institutions in 1 country.

Jarrod A CallDepartment of Medicine, University of Virginia, Charlottesville, Virginia.
Rebecca J WilsonDepartment of Medicine, University of Virginia, Charlottesville, Virginia.
Rhianna C LakerDepartment of Medicine, University of Virginia, Charlottesville, Virginia.
Mei ZhangDepartment of Medicine, University of Virginia, Charlottesville, Virginia.
Mondira KunduDepartment of Pathology, St. Jude Children's Research Hospital, Memphis, Tennessee.
Zhen YanDepartment of Medicine, University of Virginia, Charlottesville, Virginia; zhen.yan@virginia.edu.
University of Virginia · USSt. Jude Children's Research Hospital · US

Funding

p38 MAPK a regulator of muscle contraction and functionR01AR050429 · NIAMS · VIRGINIA POLYTECHNIC INST AND ST UNIV · PI YAN, ZHEN · 2005 to 2022
$5.3M
Muscle-mediated protection against MODSR01GM114840 · NIGMS · UNIVERSITY OF VIRGINIA · PI YAN, ZHEN · 2015 to 2018
$1.2M
NIAMS NIH HHS R01 AR050429NIGMS NIH HHS R01 GM114840
6 · The paper itself

Abstract

Autophagy is a conserved cellular process for degrading aggregate proteins and dysfunctional organelle. It is still debatable if autophagy and mitophagy (a specific process of autophagy of mitochondria) play important roles in myogenic differentiation and functional regeneration of skeletal muscle. We tested the hypothesis that autophagy is critical for functional regeneration of skeletal muscle. We first observed time-dependent increases (3- to 6-fold) of autophagy-related proteins (Atgs), including Ulk1, Beclin1, and LC3, along with reduced p62 expression during C2C12 differentiation, suggesting increased autophagy capacity and flux during myogenic differentiation. We then used cardiotoxin (Ctx) or ischemia-reperfusion (I/R) to induce muscle injury and regeneration and observed increases in Atgs between

Indexed as

AnimalsAutophagyAutophagy-Related Protein-1 HomologBeclin-1Cell DifferentiationCell LineCobra Cardiotoxin ProteinsGene Expression RegulationMiceMice, KnockoutMicrotubule-Associated ProteinsMitochondriaMitophagyMuscle, SkeletalMuscle StrengthMyoblasts, SkeletalAutophagy-Related Protein-1 HomologBeclin-1Becn1 protein, mouseCobra Cardiotoxin ProteinsMap1lc3b protein, mouseMicrotubule-Associated ProteinsSequestosome-1 ProteinSqstm1 protein, mouseUlk1 protein, mousemitophagymuscle repairtorqueUnc-51-like autophagy activating kinase 1

Identifiers

PMID28356270
PMCPMC5494591
OpenAlexW2604054151

What OpenQuestion holds

Textmetadata
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.