Evidence map›Paper›PMID 28260872›Full record

ArticleInternational journal of chronic obstructive pulmonary disease2017

Reduced nuclear translocation of serum response factor is associated with skeletal muscle atrophy in a cigarette smoke-induced mouse model of COPD.

Ran Ma, Xuefang Gong, Hua Jiang, Chunyi Lin, Yuqin Chen, Xiaoming Xu, Chenting Zhang, Jian Wang, Wenju Lu, Nanshan Zhong

Erratum issuedAbstract read
In one paragraph

Article in International journal of chronic obstructive pulmonary disease, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
–field-weighted citation impact
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

10 citing papers in PubMed.

  1. Review
  2. Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Smoking cessation affects the natural history of COPD.International journal of chronic obstructive pulmonary disease · 2017
    Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

10 authors.

Ran MaGuangzhou Institute of Respiratory Disease, State Key Laboratory of Respiratory Diseases, The 1st Affiliated Hospital, Guangzhou Medical University, Guangzhou, Guangdong, People's Republic of China.
Xuefang GongGuangzhou Institute of Respiratory Disease, State Key Laboratory of Respiratory Diseases, The 1st Affiliated Hospital, Guangzhou Medical University, Guangzhou, Guangdong, People's Republic of China.
Hua JiangGuangzhou Institute of Respiratory Disease, State Key Laboratory of Respiratory Diseases, The 1st Affiliated Hospital, Guangzhou Medical University, Guangzhou, Guangdong, People's Republic of China.
Chunyi LinGuangzhou Institute of Respiratory Disease, State Key Laboratory of Respiratory Diseases, The 1st Affiliated Hospital, Guangzhou Medical University, Guangzhou, Guangdong, People's Republic of China.
Yuqin ChenGuangzhou Institute of Respiratory Disease, State Key Laboratory of Respiratory Diseases, The 1st Affiliated Hospital, Guangzhou Medical University, Guangzhou, Guangdong, People's Republic of China.
Xiaoming XuGuangzhou Institute of Respiratory Disease, State Key Laboratory of Respiratory Diseases, The 1st Affiliated Hospital, Guangzhou Medical University, Guangzhou, Guangdong, People's Republic of China.
Chenting ZhangGuangzhou Institute of Respiratory Disease, State Key Laboratory of Respiratory Diseases, The 1st Affiliated Hospital, Guangzhou Medical University, Guangzhou, Guangdong, People's Republic of China.
Jian WangGuangzhou Institute of Respiratory Disease, State Key Laboratory of Respiratory Diseases, The 1st Affiliated Hospital, Guangzhou Medical University, Guangzhou, Guangdong, People's Republic of China.
Wenju LuGuangzhou Institute of Respiratory Disease, State Key Laboratory of Respiratory Diseases, The 1st Affiliated Hospital, Guangzhou Medical University, Guangzhou, Guangdong, People's Republic of China.
Nanshan ZhongGuangzhou Institute of Respiratory Disease, State Key Laboratory of Respiratory Diseases, The 1st Affiliated Hospital, Guangzhou Medical University, Guangzhou, Guangdong, People's Republic of China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Skeletal muscle atrophy and dysfunction are common complications in the chronic obstructive pulmonary disease (COPD). However, the underlying molecular mechanism remains elusive. Serum response factor (SRF) is a transcription factor which is critical in myocyte differentiation and growth. In this study, we established a mouse COPD model induced by cigarette smoking (CS) exposure for 24 weeks, with apparent pathophysiological changes, including increased airway resistance, enlarged alveoli, and skeletal muscle atrophy. Levels of upstream regulators of SRF, striated muscle activator of Rho signaling (STARS), and ras homolog gene family, member A (RhoA) were decreased in quadriceps muscle of COPD mice. Meanwhile, the nucleic location of SRF was diminished along with its cytoplasmic accumulation. There was a downregulation of the target muscle-specific gene,

Indexed as

Active Transport, Cell NucleusAnimalsCell NucleusDisease Models, AnimalGene Expression RegulationInsulin-Like Growth Factor ILungMaleMice, Inbred BALB CMicrofilament ProteinsMuscular AtrophyPulmonary Disease, Chronic ObstructiveQuadriceps MusclerhoA GTP-Binding Proteinrho GTP-Binding ProteinsSerum Response FactorAbra protein, mouseinsulin-like growth factor-1, mouseInsulin-Like Growth Factor IMicrofilament ProteinsrhoA GTP-Binding ProteinRhoA protein, mouserho GTP-Binding ProteinsSerum Response FactorSmokechronic obstructive pulmonary diseasecigarette smokingskeletal muscle atrophySRF

Identifiers

PMID28260872
PMCPMC5327903

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.