Evidence map›Paper›PMID 18441278›Full record

ReviewAmerican journal of respiratory cell and molecular biology2008

Cigarette smoke triggers code red: p21CIP1/WAF1/SDI1 switches on danger responses in the lung.

Rubin M Tuder, Jeong H Yun, Brian B Graham

Open access · greenAbstract readReview
In one paragraph

Review in American journal of respiratory cell and molecular biology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.8field-weighted citation impact, top 16% 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

14 citing papers in PubMed, 31 citations in OpenAlex.

  1. Review
  2. Genetic ablation of histone deacetylase 2 leads to lung cellular senescence and lymphoid follicle formation in COPD/emphysema.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2018
    Article
  3. Article
  4. Article
  5. Soluble extracellular Klotho decreases sensitivity to cigarette smoke induced cell death in human lung epithelial cells.Toxicology in vitro : an international journal published in association with BIBRA · 2015
    Article
  6. Senescence in chronic obstructive pulmonary disease.Proceedings of the American Thoracic Society · 2012
    Review
  7. Review
  8. Review
  9. Article
  10. Article
  11. Role of mutagenicity in asbestos fiber-induced carcinogenicity and other diseases.Journal of toxicology and environmental health. Part B, Critical reviews · 2011
    Review
  12. Article
  13. Asbestos-induced lung diseases: an update.Translational research : the journal of laboratory and clinical medicine · 2009
    Review
  14. 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

3 authors at 1 institution in 1 country.

Rubin M TuderDivision of Pulmonary Sciences and Critical Care Medicine, Department of Medicine, University of Colorado Denver, School of Medicine, 4200 East 9th Avenue, Campus Box C272, Denver, CO 80262, USA. Rubin.Tuder@UCHSC.EDU
Jeong H Yun
Brian B Graham
University of Colorado Denver · US

Funding

Endothelial Cell Death in EmphysemaR01HL066554 · NHLBI · UNIVERSITY OF COLORADO DENVER · PI TUDER, RUBIN M · 2000 to 2007
$2.6M
Schistosomiasis Associated Pulmonary Arterial HypertensionK08HL105536 · NHLBI · UNIVERSITY OF COLORADO DENVER · PI GRAHAM, BRIAN BARKLEY · 2011 to 2015
$653k
NHLBI NIH HHS HL66554NHLBI NIH HHS K08 HL105536
6 · The paper itself

Abstract

The article by Yao and coworkers in this issue (Am. J. Respir. Cell Mol. Biol. 2008;39:7-18) reveals that the cyclin-dependent kinase inhibitor p21CIP1/WAF1/SDI1 (designated hereafter as p21), which has been linked to cell cycle growth arrest due to stress or danger cell responses, may modulate alveolar inflammation and alveolar destruction, and thus enlightens our present understanding of how the lung senses injury due to cigarette smoke and integrates these responses with those that activate inflammatory pathways potentially harmful to the lung. Furthermore, the interplay of p21 and cellular processes involving cell senescence and the imbalance of cell proliferation/apoptosis may provide us with a more logical explanation of how p21, acting as a sensor of cellular stress, might have such potent and wide roles in lung responses triggered by cigarette smoke. Molecular switches, ontologically designed for the protection of the host, are now hijacked by injurious stresses (such as cigarette smoke), leading to organ damage.

Indexed as

AnimalsCellular SenescenceCyclin-Dependent Kinase Inhibitor p21EmphysemaHumansLipopolysaccharidesLungMiceMice, KnockoutN-Formylmethionine Leucyl-PhenylalaninePulmonary Disease, Chronic ObstructiveSmokingTelomereCDKN1A protein, humanCdkn1a protein, mouseCyclin-Dependent Kinase Inhibitor p21LipopolysaccharidesN-Formylmethionine Leucyl-Phenylalanine

Identifiers

PMID18441278
PMCPMC2720121
OpenAlexW1970199869

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.