Evidence map›Paper›PMID 16079187›Full record

ArticleAmerican journal of physiology. Cell physiology2005

Role of TNF-{alpha} signaling in regeneration of cardiotoxin-injured muscle.

Shuen-Ei Chen, Eric Gerken, Yingmin Zhang, Mei Zhan, Raja K Mohan, Andrew S Li, Michael B Reid, Yi-Ping Li

Open access · greenAbstract read
In one paragraph

Article in American journal of physiology. Cell physiology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 73 papers.

0numbers the graph read from it
0cells of the map it votes in
73citing papers in PubMed
2.6field-weighted citation impact, top 10% 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

73 citing papers in PubMed, 160 citations in OpenAlex.

  1. Review
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  9. Review
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  13. Review
  14. Article
  15. Skeletal Muscle Regeneration in Cardiotoxin-Induced Muscle Injury Models.International journal of molecular sciences · 2022
    Review
  16. TNFα and IFNγ cooperate for efficient pro- to anti-inflammatory transition of macrophages during muscle regeneration.Proceedings of the National Academy of Sciences of the United States of America · 2022
    Article
  17. Article
  18. Article
  19. Review
  20. Article

13 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

8 authors at 2 institutions in 1 country.

Shuen-Ei ChenDepartment of Medicine, Baylor College of Medicine, One Baylor Plaza 520B, Houston, TX 77030, USA.
Eric Gerken
Yingmin Zhang
Mei Zhan
Raja K Mohan
Andrew S Li
Michael B Reid
Yi-Ping Li
Baylor College of Medicine · USUniversity of Kentucky · US

Funding

Regulation of Skeletal Muscle RegenerationR01AR049022 · NIAMS · UNIVERSITY OF TEXAS HLTH SCI CTR HOUSTON · PI LI, YI-PING · 2003 to 2012
$3.0M
PHYSIOLOGY OF RESPIRATORY MUSCLE CELLSR01HL059878 · NHLBI · UNIVERSITY OF KENTUCKY · PI REID, MICHAEL B · 1998 to 2005
$1.4M
NHLBI NIH HHS HL-59878NHLBI NIH HHS R01 HL059878NIAMS NIH HHS AR-049022NIAMS NIH HHS R01 AR049022
6 · The paper itself

Abstract

Recent data suggest a physiological role for the proinflammatory cytokine TNF-alpha in skeletal muscle regeneration. However, the underlying mechanism is not understood. In the present study, we analyzed TNF-alpha-activated signaling pathways involved in myogenesis in soleus muscle injured by cardiotoxin (CTX) in TNF-alpha receptor double-knockout mice (p55(-/-)p75(-/-)). We found that activation of p38MAPK, which is critical for myogenesis, was blocked in CTX-injured p55(-/-)p75(-/-) soleus on day 3 postinjury when myogenic differentiation was being initiated, while activation of ERK1/2 and JNK MAPK, as well as transcription factor NF-kappaB, was not reduced. Consequently, the phosphorylation of transcription factor myocyte enhancer factor-2C, which is catalyzed by p38 and crucial for the expression of muscle-specific genes, was blunted. Meanwhile, expression of p38-dependent differentiation marker myogenin and p21 were suppressed. In addition, expression of cyclin D1 was fivefold that in wild-type (WT) soleus. These results suggest that myogenic differentiation is blocked or delayed in the absence of TNF-alpha signaling. Histological studies revealed abnormalities in regenerating p55(-/-)p75(-/-) soleus. On day 5 postinjury, new myofiber formation was clearly observed in WT soleus but not in p55(-/-)p75(-/-) soleus. To the contrary, p55(-/-)p75(-/-) soleus displayed renewed inflammation and dystrophic calcification. On day 12 postinjury, the muscle architecture of WT soleus was largely restored. Yet, in p55(-/-)p75(-/-) soleus, multifocal areas of inflammation, myofiber death, and myofibers with smaller cross-sectional area were observed. Functional studies demonstrated an attenuated recovery of contractile force in injured p55(-/-)p75(-/-) soleus. These data suggest that TNF-alpha signaling plays a critical regulatory role in muscle regeneration.

Indexed as

AnimalsCobra Cardiotoxin ProteinsEnzyme ActivationMiceMice, KnockoutMuscle ContractionMuscle DevelopmentMuscle, SkeletalMuscular Diseasesp38 Mitogen-Activated Protein KinasesReceptors, Tumor Necrosis FactorRegenerationSignal TransductionTumor Necrosis Factor-alphaCobra Cardiotoxin Proteinsp38 Mitogen-Activated Protein KinasesReceptors, Tumor Necrosis FactorTumor Necrosis Factor-alpha

Identifiers

PMID16079187
PMCPMC3099530
OpenAlexW2114596120

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.