Identifying targets for COPD treatment through gene expression analyses. Review uri icon

Overview

MeSH

  • Apoptosis
  • Cell Adhesion Molecules
  • Cell Proliferation
  • Disease Progression
  • Early Growth Response Protein 1
  • Gene Expression Profiling
  • Heme Oxygenase-1
  • Histone Deacetylases
  • Humans
  • Matrix Metalloproteinase Inhibitors
  • Matrix Metalloproteinases
  • NF-kappa B
  • Oligonucleotide Array Sequence Analysis
  • Oxidative Stress
  • Pulmonary Emphysema
  • Receptors, Chemokine
  • Smoking
  • p38 Mitogen-Activated Protein Kinases

MeSH Major

  • Pulmonary Disease, Chronic Obstructive

abstract

  • Despite the status of chronic obstructive pulmonary disease (COPD) as a major global health problem, no currently available therapies can limit COPD progression. Therefore, an urgent need exists for the development of new and effective treatments for COPD. An improved understanding in the molecular pathogenesis of COPD can potentially identify molecular targets to facilitate the development of new therapeutic modalities. Among the best approaches for understanding the molecular basis of COPD include gene expression profiling techniques, such as serial analysis of gene expression or microarrays. Using these methods, recent studies have mapped comparative gene expression profiles of lung tissues from patients with different stages of COPD relative to healthy smokers or non-smokers. Such studies have revealed a number of differentially-regulated genes associated with COPD progression, which include genes involved in the regulation of inflammation, extracellular matrix, cytokines, chemokines, apoptosis, and stress responses. These studies have shed new light on the molecular mechanisms of COPD, and suggest novel targets for clinical treatments.

publication date

  • 2008

has subject area

  • Apoptosis
  • Cell Adhesion Molecules
  • Cell Proliferation
  • Disease Progression
  • Early Growth Response Protein 1
  • Gene Expression Profiling
  • Heme Oxygenase-1
  • Histone Deacetylases
  • Humans
  • Matrix Metalloproteinase Inhibitors
  • Matrix Metalloproteinases
  • NF-kappa B
  • Oligonucleotide Array Sequence Analysis
  • Oxidative Stress
  • Pulmonary Disease, Chronic Obstructive
  • Pulmonary Emphysema
  • Receptors, Chemokine
  • Smoking
  • p38 Mitogen-Activated Protein Kinases

Research

keywords

  • Journal Article
  • Review

Identity

Language

  • eng

PubMed Central ID

  • PMC2629979

PubMed ID

  • 18990963

Additional Document Info

start page

  • 359

end page

  • 370

volume

  • 3

number

  • 3