Evidence map›Paper›PMID 16484683›Full record

ReviewAmerican journal of respiratory cell and molecular biology2006

Oxidants and signaling by mitogen-activated protein kinases in lung epithelium.

Brooke T Mossman, Karen M Lounsbury, Sekhar P Reddy

Open access · greenAbstract readReview
In one paragraph

Review in American journal of respiratory cell and molecular biology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 68 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
68citing papers in PubMed, 1 pooled it
6.8field-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

68 citing papers in PubMed, 1 synthesis or guideline pooled it, 157 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Review
  4. Article
  5. Article
  6. Article
  7. Animal models and mechanisms of tobacco smoke-induced chronic obstructive pulmonary disease (COPD).Journal of toxicology and environmental health. Part B, Critical reviews · 2023
    Review
  8. Article
  9. Targeting the EGFR-ERK axis using the compatible solute ectoine to stabilize CFTR mutant F508del.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2022
    Article
  10. Review
  11. Article
  12. Review
  13. Article
  14. Article
  15. Intracellular C3 Protects Human Airway Epithelial Cells from Stress-associated Cell Death.American journal of respiratory cell and molecular biology · 2019
    Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Review

8 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

3 authors at 1 institution in 1 country.

Brooke T MossmanDepartment of Pathology, University of Vermont College of Medicine, Burlington, VT 05405, USA. Brooke.Mossman@uvm.edu
Karen M Lounsbury
Sekhar P Reddy
University of Vermont · US

Funding

SIGNALING IN EPITHELIAL INJURY, PROLIFERATION &FIBROSISP01HL067004 · NHLBI · UNIVERSITY OF VERMONT &ST AGRIC COLLEGE · PI MOSSMAN, BROOKE TAYLOR · 2001 to 2005
$7.6M
The Role and Biology of Fra-1 in Lung Injury and RepairR01ES011863 · NIEHS · UNIVERSITY OF ILLINOIS AT CHICAGO · PI REDDY, SEKHAR P. · 2002 to 2013
$3.4M
Fra-1/Nrf2 Balance Signaling and Resolution of Inflammatory Lung InjuryR56ES011863 · NIEHS · UNIVERSITY OF ILLINOIS AT CHICAGO · PI REDDY, SEKHAR P. · 2016 to 2016
$90k
NHLBI NIH HHS HL69004NHLBI NIH HHS P01 HL067004NIEHS NIH HHS ES11863
6 · The paper itself

Abstract

Oxidants in cigarette smoke and generated from asbestos fibers activate mitogen-activated protein kinase (MAPK) signaling cascades in lung epithelial cells in vitro and in vivo. These signaling pathways lead to the enhanced ability of Jun and Fos family members (i.e., components of the activator protein [AP]-1 transcription factor) to activate transcription of a number of AP-1-dependent target genes involved in cell proliferation or death, differentiation, and inflammation. Research by the Basbaum laboratory has been critical in showing that mucin transcription in response to cigarette smoke and gram-positive bacteria is mediated through activation of the epidermal growth factor receptor and MAPK cascades. Work from our laboratories supports the concept that MAPK signaling and AP-1 transactivation by cigarette smoke and asbestos may synergize in lung epithelial cell injury, compensatory proliferation of lung epithelial cells, and carcinogenesis, supporting a mechanistic framework for the striking increases in lung cancer incidence in asbestos workers who smoke. Targeting of MAPKs and inter-related signaling cascades may be critical to the prevention of lung cancers and control of mucin overproduction in a number of lung diseases including asthma, cystic fibrosis, chronic bronchitis, and chronic obstructive pulmonary disease.

Indexed as

Signal TransductionAnimalsAsbestosCell DifferentiationEnzyme ActivationEpithelial CellsErbB ReceptorsFos-Related Antigen 1HumansLungLung NeoplasmsMineral FibersMitogen-Activated Protein KinasesMucinsNicotianaOxidantsAsbestosErbB ReceptorsFos-Related Antigen 1Mineral FibersMitogen-Activated Protein KinasesMucinsOxidantsProto-Oncogene Proteins c-fosReactive Oxygen SpeciesSmokeTranscription Factor AP-1

Identifiers

PMID16484683
PMCPMC2644227
OpenAlexW2082835152

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.