Models of chronic obstructive pulmonary disease
Identifieur interne : 000076 ( Pmc/Curation ); précédent : 000075; suivant : 000077Models of chronic obstructive pulmonary disease
Auteurs : David A. Groneberg [Allemagne] ; K Fan Chung [Royaume-Uni]Source :
- Respiratory Research [ 1465-9921 ] ; 2004.
Abstract
Chronic obstructive pulmonary disease (COPD) is a major global health problem and is predicted to become the third most common cause of death by 2020. Apart from the important preventive steps of smoking cessation, there are no other specific treatments for COPD that are as effective in reversing the condition, and therefore there is a need to understand the pathophysiological mechanisms that could lead to new therapeutic strategies. The development of experimental models will help to dissect these mechanisms at the cellular and molecular level. COPD is a disease characterized by progressive airflow obstruction of the peripheral airways, associated with lung inflammation, emphysema and mucus hypersecretion. Different approaches to mimic COPD have been developed but are limited in comparison to models of allergic asthma. COPD models usually do not mimic the major features of human COPD and are commonly based on the induction of COPD-like lesions in the lungs and airways using noxious inhalants such as tobacco smoke, nitrogen dioxide, or sulfur dioxide. Depending on the duration and intensity of exposure, these noxious stimuli induce signs of chronic inflammation and airway remodelling. Emphysema can be achieved by combining such exposure with instillation of tissue-degrading enzymes. Other approaches are based on genetically-targeted mice which develop COPD-like lesions with emphysema, and such mice provide deep insights into pathophysiological mechanisms. Future approaches should aim to mimic irreversible airflow obstruction, associated with cough and sputum production, with the possibility of inducing exacerbations.
Url:
DOI: 10.1186/1465-9921-5-18
PubMed: 15522115
PubMed Central: 533858
Links toward previous steps (curation, corpus...)
- to stream Pmc, to step Corpus: Pour aller vers cette notice dans l'étape Curation :000188
Links to Exploration step
PMC:533858Le document en format XML
<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">Models of chronic obstructive pulmonary disease</title>
<author><name sortKey="Groneberg, David A" sort="Groneberg, David A" uniqKey="Groneberg D" first="David A" last="Groneberg">David A. Groneberg</name>
<affiliation wicri:level="1"><nlm:aff id="I1">Pneumology and Immunology, Otto-Heubner-Centre, Charité School of Medicine, Free University and Humboldt-University, Berlin, Germany</nlm:aff>
<country xml:lang="fr">Allemagne</country>
<wicri:regionArea>Pneumology and Immunology, Otto-Heubner-Centre, Charité School of Medicine, Free University and Humboldt-University, Berlin</wicri:regionArea>
</affiliation>
</author>
<author><name sortKey="Chung, K Fan" sort="Chung, K Fan" uniqKey="Chung K" first="K Fan" last="Chung">K Fan Chung</name>
<affiliation wicri:level="1"><nlm:aff id="I2">Thoracic Medicine, National Heart & Lung Institute, Imperial College, London, UK</nlm:aff>
<country xml:lang="fr">Royaume-Uni</country>
<wicri:regionArea>Thoracic Medicine, National Heart & Lung Institute, Imperial College, London</wicri:regionArea>
</affiliation>
</author>
</titleStmt>
<publicationStmt><idno type="wicri:source">PMC</idno>
<idno type="pmid">15522115</idno>
<idno type="pmc">533858</idno>
<idno type="url">http://www.ncbi.nlm.nih.gov/pmc/articles/PMC533858</idno>
<idno type="RBID">PMC:533858</idno>
<idno type="doi">10.1186/1465-9921-5-18</idno>
<date when="2004">2004</date>
<idno type="wicri:Area/Pmc/Corpus">000188</idno>
<idno type="wicri:explorRef" wicri:stream="Pmc" wicri:step="Corpus" wicri:corpus="PMC">000188</idno>
<idno type="wicri:Area/Pmc/Curation">000076</idno>
<idno type="wicri:explorRef" wicri:stream="Pmc" wicri:step="Curation">000076</idno>
</publicationStmt>
<sourceDesc><biblStruct><analytic><title xml:lang="en" level="a" type="main">Models of chronic obstructive pulmonary disease</title>
<author><name sortKey="Groneberg, David A" sort="Groneberg, David A" uniqKey="Groneberg D" first="David A" last="Groneberg">David A. Groneberg</name>
<affiliation wicri:level="1"><nlm:aff id="I1">Pneumology and Immunology, Otto-Heubner-Centre, Charité School of Medicine, Free University and Humboldt-University, Berlin, Germany</nlm:aff>
<country xml:lang="fr">Allemagne</country>
<wicri:regionArea>Pneumology and Immunology, Otto-Heubner-Centre, Charité School of Medicine, Free University and Humboldt-University, Berlin</wicri:regionArea>
</affiliation>
</author>
<author><name sortKey="Chung, K Fan" sort="Chung, K Fan" uniqKey="Chung K" first="K Fan" last="Chung">K Fan Chung</name>
<affiliation wicri:level="1"><nlm:aff id="I2">Thoracic Medicine, National Heart & Lung Institute, Imperial College, London, UK</nlm:aff>
<country xml:lang="fr">Royaume-Uni</country>
<wicri:regionArea>Thoracic Medicine, National Heart & Lung Institute, Imperial College, London</wicri:regionArea>
</affiliation>
</author>
</analytic>
<series><title level="j">Respiratory Research</title>
<idno type="ISSN">1465-9921</idno>
<idno type="eISSN">1465-993X</idno>
<imprint><date when="2004">2004</date>
</imprint>
</series>
</biblStruct>
</sourceDesc>
</fileDesc>
<profileDesc><textClass></textClass>
</profileDesc>
</teiHeader>
<front><div type="abstract" xml:lang="en"><p>Chronic obstructive pulmonary disease (COPD) is a major global health problem and is predicted to become the third most common cause of death by 2020. Apart from the important preventive steps of smoking cessation, there are no other specific treatments for COPD that are as effective in reversing the condition, and therefore there is a need to understand the pathophysiological mechanisms that could lead to new therapeutic strategies. The development of experimental models will help to dissect these mechanisms at the cellular and molecular level. COPD is a disease characterized by progressive airflow obstruction of the peripheral airways, associated with lung inflammation, emphysema and mucus hypersecretion. Different approaches to mimic COPD have been developed but are limited in comparison to models of allergic asthma. COPD models usually do not mimic the major features of human COPD and are commonly based on the induction of COPD-like lesions in the lungs and airways using noxious inhalants such as tobacco smoke, nitrogen dioxide, or sulfur dioxide. Depending on the duration and intensity of exposure, these noxious stimuli induce signs of chronic inflammation and airway remodelling. Emphysema can be achieved by combining such exposure with instillation of tissue-degrading enzymes. Other approaches are based on genetically-targeted mice which develop COPD-like lesions with emphysema, and such mice provide deep insights into pathophysiological mechanisms. Future approaches should aim to mimic irreversible airflow obstruction, associated with cough and sputum production, with the possibility of inducing exacerbations.</p>
</div>
</front>
<back><div1 type="bibliography"><listBibl><biblStruct></biblStruct>
<biblStruct></biblStruct>
<biblStruct></biblStruct>
<biblStruct></biblStruct>
<biblStruct></biblStruct>
<biblStruct></biblStruct>
<biblStruct></biblStruct>
<biblStruct></biblStruct>
<biblStruct></biblStruct>
<biblStruct></biblStruct>
<biblStruct></biblStruct>
<biblStruct></biblStruct>
<biblStruct></biblStruct>
<biblStruct></biblStruct>
<biblStruct></biblStruct>
<biblStruct></biblStruct>
<biblStruct></biblStruct>
<biblStruct></biblStruct>
<biblStruct></biblStruct>
<biblStruct></biblStruct>
<biblStruct></biblStruct>
<biblStruct></biblStruct>
<biblStruct></biblStruct>
<biblStruct></biblStruct>
<biblStruct></biblStruct>
<biblStruct></biblStruct>
<biblStruct></biblStruct>
<biblStruct></biblStruct>
<biblStruct></biblStruct>
<biblStruct></biblStruct>
<biblStruct></biblStruct>
<biblStruct></biblStruct>
<biblStruct></biblStruct>
<biblStruct></biblStruct>
<biblStruct></biblStruct>
<biblStruct></biblStruct>
<biblStruct></biblStruct>
<biblStruct></biblStruct>
<biblStruct></biblStruct>
<biblStruct></biblStruct>
<biblStruct></biblStruct>
<biblStruct></biblStruct>
<biblStruct></biblStruct>
<biblStruct></biblStruct>
<biblStruct></biblStruct>
<biblStruct></biblStruct>
<biblStruct></biblStruct>
<biblStruct></biblStruct>
<biblStruct></biblStruct>
<biblStruct></biblStruct>
<biblStruct></biblStruct>
<biblStruct></biblStruct>
<biblStruct></biblStruct>
<biblStruct></biblStruct>
<biblStruct></biblStruct>
<biblStruct></biblStruct>
<biblStruct></biblStruct>
<biblStruct></biblStruct>
<biblStruct></biblStruct>
<biblStruct></biblStruct>
<biblStruct></biblStruct>
<biblStruct></biblStruct>
<biblStruct></biblStruct>
<biblStruct></biblStruct>
<biblStruct></biblStruct>
<biblStruct></biblStruct>
<biblStruct></biblStruct>
<biblStruct></biblStruct>
<biblStruct></biblStruct>
<biblStruct></biblStruct>
<biblStruct></biblStruct>
<biblStruct></biblStruct>
<biblStruct></biblStruct>
<biblStruct></biblStruct>
<biblStruct></biblStruct>
<biblStruct></biblStruct>
<biblStruct></biblStruct>
<biblStruct></biblStruct>
<biblStruct></biblStruct>
<biblStruct></biblStruct>
<biblStruct></biblStruct>
<biblStruct></biblStruct>
<biblStruct></biblStruct>
<biblStruct></biblStruct>
<biblStruct></biblStruct>
<biblStruct></biblStruct>
<biblStruct></biblStruct>
<biblStruct></biblStruct>
<biblStruct></biblStruct>
<biblStruct></biblStruct>
<biblStruct></biblStruct>
<biblStruct></biblStruct>
<biblStruct></biblStruct>
<biblStruct></biblStruct>
<biblStruct></biblStruct>
<biblStruct></biblStruct>
<biblStruct></biblStruct>
<biblStruct></biblStruct>
<biblStruct></biblStruct>
<biblStruct></biblStruct>
<biblStruct></biblStruct>
<biblStruct></biblStruct>
<biblStruct></biblStruct>
<biblStruct></biblStruct>
<biblStruct></biblStruct>
<biblStruct></biblStruct>
<biblStruct></biblStruct>
<biblStruct></biblStruct>
<biblStruct></biblStruct>
<biblStruct></biblStruct>
<biblStruct></biblStruct>
<biblStruct></biblStruct>
<biblStruct></biblStruct>
<biblStruct></biblStruct>
<biblStruct></biblStruct>
<biblStruct></biblStruct>
<biblStruct></biblStruct>
<biblStruct></biblStruct>
<biblStruct></biblStruct>
<biblStruct></biblStruct>
<biblStruct></biblStruct>
<biblStruct></biblStruct>
<biblStruct></biblStruct>
<biblStruct></biblStruct>
<biblStruct></biblStruct>
<biblStruct></biblStruct>
<biblStruct></biblStruct>
<biblStruct></biblStruct>
<biblStruct></biblStruct>
<biblStruct></biblStruct>
<biblStruct></biblStruct>
<biblStruct></biblStruct>
<biblStruct></biblStruct>
<biblStruct></biblStruct>
<biblStruct></biblStruct>
<biblStruct></biblStruct>
<biblStruct></biblStruct>
<biblStruct></biblStruct>
<biblStruct></biblStruct>
<biblStruct></biblStruct>
<biblStruct></biblStruct>
<biblStruct></biblStruct>
<biblStruct></biblStruct>
<biblStruct></biblStruct>
<biblStruct></biblStruct>
<biblStruct></biblStruct>
<biblStruct></biblStruct>
<biblStruct></biblStruct>
<biblStruct></biblStruct>
<biblStruct></biblStruct>
<biblStruct></biblStruct>
<biblStruct></biblStruct>
<biblStruct></biblStruct>
<biblStruct></biblStruct>
<biblStruct></biblStruct>
<biblStruct></biblStruct>
<biblStruct></biblStruct>
<biblStruct></biblStruct>
<biblStruct></biblStruct>
<biblStruct></biblStruct>
<biblStruct></biblStruct>
<biblStruct></biblStruct>
<biblStruct></biblStruct>
<biblStruct></biblStruct>
<biblStruct></biblStruct>
<biblStruct></biblStruct>
<biblStruct></biblStruct>
<biblStruct></biblStruct>
<biblStruct></biblStruct>
<biblStruct></biblStruct>
<biblStruct></biblStruct>
<biblStruct></biblStruct>
<biblStruct></biblStruct>
<biblStruct></biblStruct>
<biblStruct></biblStruct>
<biblStruct></biblStruct>
<biblStruct></biblStruct>
<biblStruct></biblStruct>
<biblStruct></biblStruct>
<biblStruct></biblStruct>
<biblStruct></biblStruct>
</listBibl>
</div1>
</back>
</TEI>
<pmc article-type="review-article"><pmc-dir>properties open_access</pmc-dir>
<front><journal-meta><journal-id journal-id-type="nlm-ta">Respir Res</journal-id>
<journal-title>Respiratory Research</journal-title>
<issn pub-type="ppub">1465-9921</issn>
<issn pub-type="epub">1465-993X</issn>
<publisher><publisher-name>BioMed Central</publisher-name>
</publisher>
</journal-meta>
<article-meta><article-id pub-id-type="pmid">15522115</article-id>
<article-id pub-id-type="pmc">533858</article-id>
<article-id pub-id-type="publisher-id">1465-9921-5-18</article-id>
<article-id pub-id-type="doi">10.1186/1465-9921-5-18</article-id>
<article-categories><subj-group subj-group-type="heading"><subject>Review</subject>
</subj-group>
</article-categories>
<title-group><article-title>Models of chronic obstructive pulmonary disease</article-title>
</title-group>
<contrib-group><contrib id="A1" corresp="yes" contrib-type="author"><name><surname>Groneberg</surname>
<given-names>David A</given-names>
</name>
<xref ref-type="aff" rid="I1">1</xref>
<email>david.groneberg@charite.de</email>
</contrib>
<contrib id="A2" contrib-type="author"><name><surname>Chung</surname>
<given-names>K Fan</given-names>
</name>
<xref ref-type="aff" rid="I2">2</xref>
<email>f.chung@imperial.ac.uk</email>
</contrib>
</contrib-group>
<aff id="I1"><label>1</label>
Pneumology and Immunology, Otto-Heubner-Centre, Charité School of Medicine, Free University and Humboldt-University, Berlin, Germany</aff>
<aff id="I2"><label>2</label>
Thoracic Medicine, National Heart & Lung Institute, Imperial College, London, UK</aff>
<pub-date pub-type="ppub"><year>2004</year>
</pub-date>
<pub-date pub-type="epub"><day>2</day>
<month>11</month>
<year>2004</year>
</pub-date>
<volume>5</volume>
<issue>1</issue>
<fpage>18</fpage>
<lpage>18</lpage>
<ext-link ext-link-type="uri" xlink:href="http://respiratory-research.com/content/5/1/18"></ext-link>
<history><date date-type="received"><day>28</day>
<month>7</month>
<year>2004</year>
</date>
<date date-type="accepted"><day>2</day>
<month>11</month>
<year>2004</year>
</date>
</history>
<permissions><copyright-statement>Copyright © 2004 Groneberg and Chung; licensee BioMed Central Ltd.</copyright-statement>
<copyright-year>2004</copyright-year>
<copyright-holder>Groneberg and Chung; licensee BioMed Central Ltd.</copyright-holder>
<license license-type="open-access" xlink:href="http://creativecommons.org/licenses/by/2.0"><p>This is an Open Access article distributed under the terms of the Creative Commons Attribution License (<ext-link ext-link-type="uri" xlink:href="http://creativecommons.org/licenses/by/2.0"></ext-link>
), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.</p>
<pmc-comment>
Groneberg
A
David
david.groneberg@charite.de
Models of chronic obstructive pulmonary disease
2004 Respiratory Research 5(1): 18-. (2004) 1465-9921(2004)5:1<18> urn:ISSN:1465-9921 </pmc-comment>
</license>
</permissions>
<abstract><p>Chronic obstructive pulmonary disease (COPD) is a major global health problem and is predicted to become the third most common cause of death by 2020. Apart from the important preventive steps of smoking cessation, there are no other specific treatments for COPD that are as effective in reversing the condition, and therefore there is a need to understand the pathophysiological mechanisms that could lead to new therapeutic strategies. The development of experimental models will help to dissect these mechanisms at the cellular and molecular level. COPD is a disease characterized by progressive airflow obstruction of the peripheral airways, associated with lung inflammation, emphysema and mucus hypersecretion. Different approaches to mimic COPD have been developed but are limited in comparison to models of allergic asthma. COPD models usually do not mimic the major features of human COPD and are commonly based on the induction of COPD-like lesions in the lungs and airways using noxious inhalants such as tobacco smoke, nitrogen dioxide, or sulfur dioxide. Depending on the duration and intensity of exposure, these noxious stimuli induce signs of chronic inflammation and airway remodelling. Emphysema can be achieved by combining such exposure with instillation of tissue-degrading enzymes. Other approaches are based on genetically-targeted mice which develop COPD-like lesions with emphysema, and such mice provide deep insights into pathophysiological mechanisms. Future approaches should aim to mimic irreversible airflow obstruction, associated with cough and sputum production, with the possibility of inducing exacerbations.</p>
</abstract>
<kwd-group><kwd>Chronic obstructive pulmonary disease</kwd>
<kwd>COPD</kwd>
<kwd>asthma</kwd>
<kwd>animal</kwd>
<kwd>mice</kwd>
<kwd>rat</kwd>
<kwd>guinea pig</kwd>
<kwd>tobacco smoke</kwd>
<kwd>nitrogen dioxide</kwd>
<kwd>sulfur dioxide</kwd>
</kwd-group>
</article-meta>
</front>
</pmc>
</record>
Pour manipuler ce document sous Unix (Dilib)
EXPLOR_STEP=$WICRI_ROOT/Wicri/Psychologie/explor/DanceTherParkinsonV1/Data/Pmc/Curation
HfdSelect -h $EXPLOR_STEP/biblio.hfd -nk 000076 | SxmlIndent | more
Ou
HfdSelect -h $EXPLOR_AREA/Data/Pmc/Curation/biblio.hfd -nk 000076 | SxmlIndent | more
Pour mettre un lien sur cette page dans le réseau Wicri
{{Explor lien |wiki= Wicri/Psychologie |area= DanceTherParkinsonV1 |flux= Pmc |étape= Curation |type= RBID |clé= PMC:533858 |texte= Models of chronic obstructive pulmonary disease }}
Pour générer des pages wiki
HfdIndexSelect -h $EXPLOR_AREA/Data/Pmc/Curation/RBID.i -Sk "pubmed:15522115" \ | HfdSelect -Kh $EXPLOR_AREA/Data/Pmc/Curation/biblio.hfd \ | NlmPubMed2Wicri -a DanceTherParkinsonV1
This area was generated with Dilib version V0.6.35. |