Mechanisms of pulmonary fibrosis

Tissue injury evokes highly conserved, tightly regulated inflammatory responses and less well-understood host repair responses. Both inflammation and repair involve the recruitment, activation, apoptosis, and eventual clearance of key effector cells. In this review, we propose the concept of pulmona...

Ausführliche Beschreibung

Gespeichert in:
Bibliographische Detailangaben
Veröffentlicht in:Annual review of medicine 2004-01, Vol.55 (1), p.395-417
Hauptverfasser: Thannickal, Victor J, Toews, Galen B, White, Eric S, Lynch, 3rd, Joseph P, Martinez, Fernando J
Format: Artikel
Sprache:eng
Schlagworte:
Online-Zugang:Volltext
Tags: Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
container_end_page 417
container_issue 1
container_start_page 395
container_title Annual review of medicine
container_volume 55
creator Thannickal, Victor J
Toews, Galen B
White, Eric S
Lynch, 3rd, Joseph P
Martinez, Fernando J
description Tissue injury evokes highly conserved, tightly regulated inflammatory responses and less well-understood host repair responses. Both inflammation and repair involve the recruitment, activation, apoptosis, and eventual clearance of key effector cells. In this review, we propose the concept of pulmonary fibrosis as a dysregulated repair process that is perpetually "turned on" even though classical inflammatory pathways may be dampened or "switched off." Significant regional heterogeneity, with varied histopathological patterns of inflammation and fibrosis, has been observed in individual patients with idiopathic pulmonary fibrosis. We discuss environmental factors and host response factors, such as genetic susceptibility and age, that may influence these varied manifestations. Better understanding of the mechanisms of lung repair, which include alveolar reepithelialization, myofibroblast differentiation/activation, and apoptosis, should offer more effective therapeutic options for progressive pulmonary fibrosis.
doi_str_mv 10.1146/annurev.med.55.091902.103810
format Article
fullrecord <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_80125056</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>579093921</sourcerecordid><originalsourceid>FETCH-LOGICAL-a470t-9d07be84280516ed9dcdf0eec332fcd6ddd9b6b80e7057bd5857569ed22f0d6a3</originalsourceid><addsrcrecordid>eNpdkMtKxDAUhoMozjj6ClJE3LWe3BNwI4M3GHGj4C6kTYIdehkbK_j2Zmhx4epsvv-c838IXWIoMGbi2nbdOPjvovWu4LwAjTWQAgNVGA7QEnPGc0rE-yFaAgiRM4L1Ap3EuAUATak6RgvMJBOcqCXKnn31Ybs6tjHrQ7Ybm7bv7PCThboc-ljHU3QUbBP92TxX6O3-7nX9mG9eHp7Wt5vcMglfuXYgS68YUcCx8E67ygXwvqKUhMoJ55wuRanAS-CydFxxyYX2jpAATli6QlfT3t3Qf44-fpm2jpVvGtv5foxGASYcuEjgxT9w249Dl34zhBBBpRYsQTcTVKUScfDB7Ia6Tb0MBrPXaGaNJmk0nJtJo5k0pvj5fGMs98BfePZGfwFvIXEm</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>222637964</pqid></control><display><type>article</type><title>Mechanisms of pulmonary fibrosis</title><source>Annual Reviews</source><source>MEDLINE</source><creator>Thannickal, Victor J ; Toews, Galen B ; White, Eric S ; Lynch, 3rd, Joseph P ; Martinez, Fernando J</creator><creatorcontrib>Thannickal, Victor J ; Toews, Galen B ; White, Eric S ; Lynch, 3rd, Joseph P ; Martinez, Fernando J</creatorcontrib><description>Tissue injury evokes highly conserved, tightly regulated inflammatory responses and less well-understood host repair responses. Both inflammation and repair involve the recruitment, activation, apoptosis, and eventual clearance of key effector cells. In this review, we propose the concept of pulmonary fibrosis as a dysregulated repair process that is perpetually "turned on" even though classical inflammatory pathways may be dampened or "switched off." Significant regional heterogeneity, with varied histopathological patterns of inflammation and fibrosis, has been observed in individual patients with idiopathic pulmonary fibrosis. We discuss environmental factors and host response factors, such as genetic susceptibility and age, that may influence these varied manifestations. Better understanding of the mechanisms of lung repair, which include alveolar reepithelialization, myofibroblast differentiation/activation, and apoptosis, should offer more effective therapeutic options for progressive pulmonary fibrosis.</description><identifier>ISSN: 0066-4219</identifier><identifier>EISSN: 1545-326X</identifier><identifier>DOI: 10.1146/annurev.med.55.091902.103810</identifier><identifier>PMID: 14746528</identifier><language>eng</language><publisher>United States: Annual Reviews, Inc</publisher><subject>Cystic fibrosis ; Genetics ; Humans ; Lung - immunology ; Lung - pathology ; Lung - physiopathology ; Lungs ; Medical research ; Pulmonary Fibrosis - etiology ; Pulmonary Fibrosis - pathology ; Pulmonary Fibrosis - physiopathology</subject><ispartof>Annual review of medicine, 2004-01, Vol.55 (1), p.395-417</ispartof><rights>Copyright Annual Reviews, Inc. 2004</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-a470t-9d07be84280516ed9dcdf0eec332fcd6ddd9b6b80e7057bd5857569ed22f0d6a3</citedby><cites>FETCH-LOGICAL-a470t-9d07be84280516ed9dcdf0eec332fcd6ddd9b6b80e7057bd5857569ed22f0d6a3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,4182,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/14746528$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Thannickal, Victor J</creatorcontrib><creatorcontrib>Toews, Galen B</creatorcontrib><creatorcontrib>White, Eric S</creatorcontrib><creatorcontrib>Lynch, 3rd, Joseph P</creatorcontrib><creatorcontrib>Martinez, Fernando J</creatorcontrib><title>Mechanisms of pulmonary fibrosis</title><title>Annual review of medicine</title><addtitle>Annu Rev Med</addtitle><description>Tissue injury evokes highly conserved, tightly regulated inflammatory responses and less well-understood host repair responses. Both inflammation and repair involve the recruitment, activation, apoptosis, and eventual clearance of key effector cells. In this review, we propose the concept of pulmonary fibrosis as a dysregulated repair process that is perpetually "turned on" even though classical inflammatory pathways may be dampened or "switched off." Significant regional heterogeneity, with varied histopathological patterns of inflammation and fibrosis, has been observed in individual patients with idiopathic pulmonary fibrosis. We discuss environmental factors and host response factors, such as genetic susceptibility and age, that may influence these varied manifestations. Better understanding of the mechanisms of lung repair, which include alveolar reepithelialization, myofibroblast differentiation/activation, and apoptosis, should offer more effective therapeutic options for progressive pulmonary fibrosis.</description><subject>Cystic fibrosis</subject><subject>Genetics</subject><subject>Humans</subject><subject>Lung - immunology</subject><subject>Lung - pathology</subject><subject>Lung - physiopathology</subject><subject>Lungs</subject><subject>Medical research</subject><subject>Pulmonary Fibrosis - etiology</subject><subject>Pulmonary Fibrosis - pathology</subject><subject>Pulmonary Fibrosis - physiopathology</subject><issn>0066-4219</issn><issn>1545-326X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2004</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>8G5</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><sourceid>GUQSH</sourceid><sourceid>M2O</sourceid><recordid>eNpdkMtKxDAUhoMozjj6ClJE3LWe3BNwI4M3GHGj4C6kTYIdehkbK_j2Zmhx4epsvv-c838IXWIoMGbi2nbdOPjvovWu4LwAjTWQAgNVGA7QEnPGc0rE-yFaAgiRM4L1Ap3EuAUATak6RgvMJBOcqCXKnn31Ybs6tjHrQ7Ybm7bv7PCThboc-ljHU3QUbBP92TxX6O3-7nX9mG9eHp7Wt5vcMglfuXYgS68YUcCx8E67ygXwvqKUhMoJ55wuRanAS-CydFxxyYX2jpAATli6QlfT3t3Qf44-fpm2jpVvGtv5foxGASYcuEjgxT9w249Dl34zhBBBpRYsQTcTVKUScfDB7Ia6Tb0MBrPXaGaNJmk0nJtJo5k0pvj5fGMs98BfePZGfwFvIXEm</recordid><startdate>20040101</startdate><enddate>20040101</enddate><creator>Thannickal, Victor J</creator><creator>Toews, Galen B</creator><creator>White, Eric S</creator><creator>Lynch, 3rd, Joseph P</creator><creator>Martinez, Fernando J</creator><general>Annual Reviews, Inc</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7QP</scope><scope>7T5</scope><scope>7TO</scope><scope>7U9</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>88G</scope><scope>88I</scope><scope>8AF</scope><scope>8AO</scope><scope>8FD</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>8G5</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>GUQSH</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>M2M</scope><scope>M2O</scope><scope>M2P</scope><scope>MBDVC</scope><scope>P64</scope><scope>PADUT</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>PSYQQ</scope><scope>Q9U</scope><scope>RC3</scope><scope>7X8</scope></search><sort><creationdate>20040101</creationdate><title>Mechanisms of pulmonary fibrosis</title><author>Thannickal, Victor J ; Toews, Galen B ; White, Eric S ; Lynch, 3rd, Joseph P ; Martinez, Fernando J</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-a470t-9d07be84280516ed9dcdf0eec332fcd6ddd9b6b80e7057bd5857569ed22f0d6a3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2004</creationdate><topic>Cystic fibrosis</topic><topic>Genetics</topic><topic>Humans</topic><topic>Lung - immunology</topic><topic>Lung - pathology</topic><topic>Lung - physiopathology</topic><topic>Lungs</topic><topic>Medical research</topic><topic>Pulmonary Fibrosis - etiology</topic><topic>Pulmonary Fibrosis - pathology</topic><topic>Pulmonary Fibrosis - physiopathology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Thannickal, Victor J</creatorcontrib><creatorcontrib>Toews, Galen B</creatorcontrib><creatorcontrib>White, Eric S</creatorcontrib><creatorcontrib>Lynch, 3rd, Joseph P</creatorcontrib><creatorcontrib>Martinez, Fernando J</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Calcium &amp; Calcified Tissue Abstracts</collection><collection>Immunology Abstracts</collection><collection>Oncogenes and Growth Factors Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Health &amp; Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Psychology Database (Alumni)</collection><collection>Science Database (Alumni Edition)</collection><collection>STEM Database</collection><collection>ProQuest Pharma Collection</collection><collection>Technology Research Database</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>Research Library (Alumni Edition)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Engineering Research Database</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>Research Library Prep</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health &amp; Medical Complete (Alumni)</collection><collection>Health &amp; Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Psychology Database</collection><collection>Research Library</collection><collection>Science Database</collection><collection>Research Library (Corporate)</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Research Library China</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>ProQuest One Psychology</collection><collection>ProQuest Central Basic</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Annual review of medicine</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Thannickal, Victor J</au><au>Toews, Galen B</au><au>White, Eric S</au><au>Lynch, 3rd, Joseph P</au><au>Martinez, Fernando J</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Mechanisms of pulmonary fibrosis</atitle><jtitle>Annual review of medicine</jtitle><addtitle>Annu Rev Med</addtitle><date>2004-01-01</date><risdate>2004</risdate><volume>55</volume><issue>1</issue><spage>395</spage><epage>417</epage><pages>395-417</pages><issn>0066-4219</issn><eissn>1545-326X</eissn><abstract>Tissue injury evokes highly conserved, tightly regulated inflammatory responses and less well-understood host repair responses. Both inflammation and repair involve the recruitment, activation, apoptosis, and eventual clearance of key effector cells. In this review, we propose the concept of pulmonary fibrosis as a dysregulated repair process that is perpetually "turned on" even though classical inflammatory pathways may be dampened or "switched off." Significant regional heterogeneity, with varied histopathological patterns of inflammation and fibrosis, has been observed in individual patients with idiopathic pulmonary fibrosis. We discuss environmental factors and host response factors, such as genetic susceptibility and age, that may influence these varied manifestations. Better understanding of the mechanisms of lung repair, which include alveolar reepithelialization, myofibroblast differentiation/activation, and apoptosis, should offer more effective therapeutic options for progressive pulmonary fibrosis.</abstract><cop>United States</cop><pub>Annual Reviews, Inc</pub><pmid>14746528</pmid><doi>10.1146/annurev.med.55.091902.103810</doi><tpages>23</tpages></addata></record>
fulltext fulltext
identifier ISSN: 0066-4219
ispartof Annual review of medicine, 2004-01, Vol.55 (1), p.395-417
issn 0066-4219
1545-326X
language eng
recordid cdi_proquest_miscellaneous_80125056
source Annual Reviews; MEDLINE
subjects Cystic fibrosis
Genetics
Humans
Lung - immunology
Lung - pathology
Lung - physiopathology
Lungs
Medical research
Pulmonary Fibrosis - etiology
Pulmonary Fibrosis - pathology
Pulmonary Fibrosis - physiopathology
title Mechanisms of pulmonary fibrosis
url https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2024-12-26T07%3A46%3A01IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_cross&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Mechanisms%20of%20pulmonary%20fibrosis&rft.jtitle=Annual%20review%20of%20medicine&rft.au=Thannickal,%20Victor%20J&rft.date=2004-01-01&rft.volume=55&rft.issue=1&rft.spage=395&rft.epage=417&rft.pages=395-417&rft.issn=0066-4219&rft.eissn=1545-326X&rft_id=info:doi/10.1146/annurev.med.55.091902.103810&rft_dat=%3Cproquest_cross%3E579093921%3C/proquest_cross%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=222637964&rft_id=info:pmid/14746528&rfr_iscdi=true