Apoptosis as a therapeutic target for the treatment of lung disease

Patricia M. de Souza; Mark A. Lindsay

doi:10.1016/j.coph.2005.01.012

Apoptosis as a therapeutic target for the treatment of lung disease

Patricia M. de Souza, Mark A. Lindsay

Imperial College London

Research output: Contribution to journal › Review article › peer-review

31 Citations (SciVal)

Abstract

It has been speculated that the destruction of lung tissue, associated with several acute and chronic diseases, is in part mediated through apoptosis or programmed cell death. Thus, it has been shown that both increased endothelial/epithelial cell apoptosis and decreased cell death of inflammatory cells are associated with acute lung injury/acute respiratory distress syndrome, chronic obstructive pulmonary disease, asthma and pulmonary fibrosis. In the light of these observations, it might be possible to use apoptosis modulation as a novel therapeutic approach to the treatment of lung disease.

Original language	English
Pages (from-to)	232-237
Number of pages	6
Journal	Current Opinion in Pharmacology
Volume	5
Issue number	3 SPEC. ISS.
DOIs	https://doi.org/10.1016/j.coph.2005.01.012
Publication status	Published - 30 Jun 2005

Bibliographical note

Funding Information:
Mark A Lindsay is supported by GlaxoSmithKline and Wellcome Trust (GR076111) and Patricia M de Souza by Asthma UK (03/070).

ASJC Scopus subject areas

Pharmacology
Drug Discovery

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10.1016/j.coph.2005.01.012

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title = "Apoptosis as a therapeutic target for the treatment of lung disease",

abstract = "It has been speculated that the destruction of lung tissue, associated with several acute and chronic diseases, is in part mediated through apoptosis or programmed cell death. Thus, it has been shown that both increased endothelial/epithelial cell apoptosis and decreased cell death of inflammatory cells are associated with acute lung injury/acute respiratory distress syndrome, chronic obstructive pulmonary disease, asthma and pulmonary fibrosis. In the light of these observations, it might be possible to use apoptosis modulation as a novel therapeutic approach to the treatment of lung disease.",

author = "{de Souza}, {Patricia M.} and Lindsay, {Mark A.}",

note = "Funding Information: Mark A Lindsay is supported by GlaxoSmithKline and Wellcome Trust (GR076111) and Patricia M de Souza by Asthma UK (03/070).",

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AU - Lindsay, Mark A.

N1 - Funding Information: Mark A Lindsay is supported by GlaxoSmithKline and Wellcome Trust (GR076111) and Patricia M de Souza by Asthma UK (03/070).

PY - 2005/6/30

Y1 - 2005/6/30

N2 - It has been speculated that the destruction of lung tissue, associated with several acute and chronic diseases, is in part mediated through apoptosis or programmed cell death. Thus, it has been shown that both increased endothelial/epithelial cell apoptosis and decreased cell death of inflammatory cells are associated with acute lung injury/acute respiratory distress syndrome, chronic obstructive pulmonary disease, asthma and pulmonary fibrosis. In the light of these observations, it might be possible to use apoptosis modulation as a novel therapeutic approach to the treatment of lung disease.

AB - It has been speculated that the destruction of lung tissue, associated with several acute and chronic diseases, is in part mediated through apoptosis or programmed cell death. Thus, it has been shown that both increased endothelial/epithelial cell apoptosis and decreased cell death of inflammatory cells are associated with acute lung injury/acute respiratory distress syndrome, chronic obstructive pulmonary disease, asthma and pulmonary fibrosis. In the light of these observations, it might be possible to use apoptosis modulation as a novel therapeutic approach to the treatment of lung disease.

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U2 - 10.1016/j.coph.2005.01.012

DO - 10.1016/j.coph.2005.01.012

M3 - Review article

C2 - 15907908

AN - SCOPUS:18744396141

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JO - Current Opinion in Pharmacology

JF - Current Opinion in Pharmacology

IS - 3 SPEC. ISS.

ER -

Apoptosis as a therapeutic target for the treatment of lung disease

Abstract

Bibliographical note

ASJC Scopus subject areas

Access to Document

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