Evidence map›Paper›PMID 23695700›Full record

ArticleNature communications2013

Prothymosin α overexpression contributes to the development of pulmonary emphysema.

Bing-Hua Su, Yau-Lin Tseng, Gia-Shing Shieh, Yi-Cheng Chen, Ya-Chieh Shiang, Pensee Wu, Kuo-Jung Li, Te-Hsin Yen, Ai-Li Shiau, Chao-Liang Wu

Open access · hybridAbstract read
In one paragraph

Article in Nature communications, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing 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

22 citing papers in PubMed, 39 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Review
  10. Article
  11. Article
  12. Article
  13. Prothymosin α promotes STAT3 acetylation to induce cystogenesis in Pkd1-deficient mice.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2019
    Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Review
  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

10 authors at 3 institutions in 2 countries.

Bing-Hua SuDepartment of Biochemistry and Molecular Biology, National Cheng Kung University Medical College, Tainan 70101, Taiwan.
Yau-Lin Tseng
Gia-Shing Shieh
Yi-Cheng Chen
Ya-Chieh Shiang
Pensee Wu
Kuo-Jung Li
Te-Hsin Yen
Ai-Li Shiau
Chao-Liang Wu
National Cheng Kung University · TWImperial College London · GBTainan Municipal Hospital · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Emphysema is one of the disease conditions that comprise chronic obstructive pulmonary disease. Prothymosin α transgenic mice exhibit an emphysema phenotype, but the pathophysiological role of prothymosin α in emphysema remains unclear. Here we show that prothymosin α contributes to the pathogenesis of emphysema by increasing acetylation of histones and nuclear factor-kappaB, particularly upon cigarette smoke exposure. We find a positive correlation between prothymosin α levels and the severity of emphysema in prothymosin α transgenic mice and emphysema patients. Prothymosin α overexpression increases susceptibility to cigarette smoke-induced emphysema, and cigarette smoke exposure further enhances prothymosin α expression. We show that prothymosin α inhibits the association of histone deacetylases with histones and nuclear factor-kappaB, and that prothymosin α overexpression increases expression of nuclear factor-kappaB-dependent matrix metalloproteinase 2 and matrix metalloproteinase 9, which are found in the lungs of patients with chronic obstructive pulmonary disease. These results demonstrate the clinical relevance of prothymosin α in regulating acetylation events during the pathogenesis of emphysema.

Indexed as

AcetylationAnimalsCell LineEpitheliumHistone DeacetylasesHumansLungMatrix Metalloproteinase 2Matrix Metalloproteinase 9MiceMice, TransgenicModels, BiologicalNF-kappa BPhenotypeProtein PrecursorsPulmonary EmphysemaHistone DeacetylasesMatrix Metalloproteinase 2Matrix Metalloproteinase 9NF-kappa BProtein Precursorsprothymosin alphaThymosin

Identifiers

PMID23695700
PMCPMC3674284
OpenAlexW2038011717

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.