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Identifying targets for COPD treatment through gene expression analyses.

Chen ZH, Kim HP, Ryter SW, Choi AM - Int J Chron Obstruct Pulmon Dis (2008)

Bottom Line: 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.

View Article: PubMed Central - PubMed

Affiliation: Division of Pulmonary, Allergy and Critical Care Medicine, Department of Medicine, University of Pittsburgh, Pittsburgh, PA, USA.

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.

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Molecular Mechanisms in COPD pathogenesis and potential therapeutic targets. A number of signaling pathway components have been identified which regulate apoptosis, inflammation and fibrosis potentially associated with COPD pathogenesis. Many of these have been identified as possible targets for therapeutic intervention using small molecule inhibitors or antagonists.Abbreviations: COPD, chronic obstructive pulmonary disease; ECM, extracellular matrix; Egr-1, early growth response-1; HDAC, histone deacetylase; HO-1, heme oxygenase-1; Keap-1, Kelch-like ECH associating protein-1; MMP, matrix metalloproteinase; NF-κB, nuclear factor-kappa-B; Nrf-2, nuclear factor-E2-related factor-2; p38 MAPK, p38 mitogen-activated protein kinase; ROS, reactive oxygen species; TGFβ1, transforming growth factor-B1.
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f1-copd-3-359: Molecular Mechanisms in COPD pathogenesis and potential therapeutic targets. A number of signaling pathway components have been identified which regulate apoptosis, inflammation and fibrosis potentially associated with COPD pathogenesis. Many of these have been identified as possible targets for therapeutic intervention using small molecule inhibitors or antagonists.Abbreviations: COPD, chronic obstructive pulmonary disease; ECM, extracellular matrix; Egr-1, early growth response-1; HDAC, histone deacetylase; HO-1, heme oxygenase-1; Keap-1, Kelch-like ECH associating protein-1; MMP, matrix metalloproteinase; NF-κB, nuclear factor-kappa-B; Nrf-2, nuclear factor-E2-related factor-2; p38 MAPK, p38 mitogen-activated protein kinase; ROS, reactive oxygen species; TGFβ1, transforming growth factor-B1.

Mentions: The lack of drug development for this disease is due to the relatively recent emergence of research addressing the molecular and cellular basis of COPD (Barnes et al 2003; Barnes 2005; Barnes and Hansel 2004; Donnelly and Barnes 2006;Yoshida and Tuder 2006). A general scheme of the molecular pathways involved in COPD pathogenesis and potential areas for therapeutic intervention is shown in Figure 1.


Identifying targets for COPD treatment through gene expression analyses.

Chen ZH, Kim HP, Ryter SW, Choi AM - Int J Chron Obstruct Pulmon Dis (2008)

Molecular Mechanisms in COPD pathogenesis and potential therapeutic targets. A number of signaling pathway components have been identified which regulate apoptosis, inflammation and fibrosis potentially associated with COPD pathogenesis. Many of these have been identified as possible targets for therapeutic intervention using small molecule inhibitors or antagonists.Abbreviations: COPD, chronic obstructive pulmonary disease; ECM, extracellular matrix; Egr-1, early growth response-1; HDAC, histone deacetylase; HO-1, heme oxygenase-1; Keap-1, Kelch-like ECH associating protein-1; MMP, matrix metalloproteinase; NF-κB, nuclear factor-kappa-B; Nrf-2, nuclear factor-E2-related factor-2; p38 MAPK, p38 mitogen-activated protein kinase; ROS, reactive oxygen species; TGFβ1, transforming growth factor-B1.
© Copyright Policy
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC2629979&req=5

f1-copd-3-359: Molecular Mechanisms in COPD pathogenesis and potential therapeutic targets. A number of signaling pathway components have been identified which regulate apoptosis, inflammation and fibrosis potentially associated with COPD pathogenesis. Many of these have been identified as possible targets for therapeutic intervention using small molecule inhibitors or antagonists.Abbreviations: COPD, chronic obstructive pulmonary disease; ECM, extracellular matrix; Egr-1, early growth response-1; HDAC, histone deacetylase; HO-1, heme oxygenase-1; Keap-1, Kelch-like ECH associating protein-1; MMP, matrix metalloproteinase; NF-κB, nuclear factor-kappa-B; Nrf-2, nuclear factor-E2-related factor-2; p38 MAPK, p38 mitogen-activated protein kinase; ROS, reactive oxygen species; TGFβ1, transforming growth factor-B1.
Mentions: The lack of drug development for this disease is due to the relatively recent emergence of research addressing the molecular and cellular basis of COPD (Barnes et al 2003; Barnes 2005; Barnes and Hansel 2004; Donnelly and Barnes 2006;Yoshida and Tuder 2006). A general scheme of the molecular pathways involved in COPD pathogenesis and potential areas for therapeutic intervention is shown in Figure 1.

Bottom Line: 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.

View Article: PubMed Central - PubMed

Affiliation: Division of Pulmonary, Allergy and Critical Care Medicine, Department of Medicine, University of Pittsburgh, Pittsburgh, PA, USA.

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.

Show MeSH
Related in: MedlinePlus