Evidence map›Paper›PMID 18046891›Full record

ReviewInternational journal of chronic obstructive pulmonary disease2006

Emerging role of MAP kinase pathways as therapeutic targets in COPD.

Becky A Mercer, Jeanine M D'Armiento

Open access · greenAbstract readReview
In one paragraph

Review in International journal of chronic obstructive pulmonary disease, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers.

0numbers the graph read from it
0cells of the map it votes in
51citing papers in PubMed
0.7field-weighted citation impact, top 26% 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

51 citing papers in PubMed, 115 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Review
  6. The MAPK Response to Virus Infection Is Modified by Probenecid.Current issues in molecular biology · 2025
    Review
  7. Review
  8. Review
  9. Review
  10. Article
  11. Review
  12. Article
  13. Circular RNAs: emerging players in asthma and COPD.Frontiers in cell and developmental biology · 2023
    Review
  14. Article
  15. Article
  16. Antioxidants (Basel, Switzerland) · 2022
    Article
  17. Review
  18. Current views in chronic obstructive pulmonary disease pathogenesis and management.Saudi pharmaceutical journal : SPJ : the official publication of the Saudi Pharmaceutical Society · 2021
    Review
  19. Article
  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

2 authors at 1 institution in 2 countries.

Becky A MercerInstitute of Human Nutrition, Division of Molecular Medicine, Department of Medicine, Columbia University College of Physicians and Surgeons, New York 10032, USA. bam55@columbia.edu
Jeanine M D'Armiento
Columbia University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Studies examining the cellular mechanisms of inflammation and protease production in the lung tissue and airways of COPD patients have shed light on the important role of kinase-based signaling cascades. These pathways can be activated by environmental stimuli such as tobacco smoke, and by endogenous signals such as cytokines, growth factors, and inflammation-derived oxidants. The three most widely characterized cascades are those directed by the classical mitogen activated protein (MAP) kinase (ERK1/2), stress activated protein kinase/c-Jun N-terminal protein kinase, and p38 enzymes. These phosphorylation cascades transmit and amplify extracellular, receptor-mediated signals through the cytoplasm of the cell to activate nuclear transcription factors which bind and induce expression of target genes. The result is tight control of diverse cellular events, and rapid responses to external stimuli. However, recent research suggests that constitutive or aberrant activation of MAP kinases contributes to several COPD-associated phenotypes, including mucus overproduction and secretion, inflammation, cytokine expression, apoptosis, T cell activation, matrix metalloproteinase production, and fibrosis. This review explores the biological functions of the MAP kinase pathways in the pathogenesis of COPD, their activation by cigarette smoke, and discusses the potential role of MAP kinase inhibitors in COPD therapy.

Indexed as

ApoptosisExtracellular Signal-Regulated MAP KinasesHumansJNK Mitogen-Activated Protein KinasesLungp38 Mitogen-Activated Protein KinasesPulmonary Disease, Chronic ObstructiveSmokingExtracellular Signal-Regulated MAP KinasesJNK Mitogen-Activated Protein Kinasesp38 Mitogen-Activated Protein Kinases

Identifiers

PMID18046891
PMCPMC2706609
OpenAlexW2091561566

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.