Common and unique mechanisms regulate fibrosis in various fibroproliferative diseases
Fibroproliferative diseases, including the pulmonary fibroses, systemic sclerosis, liver cirrhosis, cardiovascular disease, progressive kidney disease, and macular degeneration, are a leading cause of morbidity and mortality and can affect all tissues and organ systems. Fibrotic tissue remodeling ca...
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| Veröffentlicht in: | The Journal of clinical investigation 2007-03, Vol.117 (3), p.524-529 |
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| description | Fibroproliferative diseases, including the pulmonary fibroses, systemic sclerosis, liver cirrhosis, cardiovascular disease, progressive kidney disease, and macular degeneration, are a leading cause of morbidity and mortality and can affect all tissues and organ systems. Fibrotic tissue remodeling can also influence cancer metastasis and accelerate chronic graft rejection in transplant recipients. Nevertheless, despite its enormous impact on human health, there are currently no approved treatments that directly target the mechanism(s) of fibrosis. The primary goals of this Review series on fibrotic diseases are to discuss some of the major fibroproliferative diseases and to identify the common and unique mechanisms of fibrogenesis that might be exploited in the development of effective antifibrotic therapies. |
| doi_str_mv | 10.1172/JCI31487 |
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Fibrotic tissue remodeling can also influence cancer metastasis and accelerate chronic graft rejection in transplant recipients. Nevertheless, despite its enormous impact on human health, there are currently no approved treatments that directly target the mechanism(s) of fibrosis. The primary goals of this Review series on fibrotic diseases are to discuss some of the major fibroproliferative diseases and to identify the common and unique mechanisms of fibrogenesis that might be exploited in the development of effective antifibrotic therapies.</description><identifier>ISSN: 0021-9738</identifier><identifier>EISSN: 1558-8238</identifier><identifier>DOI: 10.1172/JCI31487</identifier><identifier>PMID: 17332879</identifier><language>eng</language><publisher>United States: American Society for Clinical Investigation</publisher><subject>Analysis ; Angiotensin II - physiology ; Biomedical research ; Blood vessels ; Bone marrow ; Cardiovascular diseases ; Cell Proliferation ; Chemokines ; Chronic Disease ; Collagen ; Connective tissue ; Cytokines ; Disease ; Embryonic Stem Cells - transplantation ; Fibroblasts ; Fibroblasts - pathology ; Fibroblasts - physiology ; Fibrosis ; Fibrosis - etiology ; Fibrosis - immunology ; Fibrosis - therapy ; Growth factors ; Humans ; Infection - immunology ; Inflammation ; Kidney diseases ; Leukocytes ; Liver cirrhosis ; Macular degeneration ; Morbidity ; Mortality ; Neovascularization, Pathologic - immunology ; Neovascularization, Pathologic - metabolism ; Neutrophils ; Pulmonary fibrosis ; Review Series ; Scleroderma ; Scleroderma (Disease) ; Systemic scleroderma ; Transforming Growth Factor beta1 - physiology ; Wound Healing</subject><ispartof>The Journal of clinical investigation, 2007-03, Vol.117 (3), p.524-529</ispartof><rights>COPYRIGHT 2007 American Society for Clinical Investigation</rights><rights>Copyright American Society for Clinical Investigation Mar 2007</rights><rights>Copyright © 2007, American Society for Clinical Investigation 2007</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c612t-1cb5553120398184ab6fb24d7850124d8901e9cc78aa8cefd1580b9cbe9ad9783</citedby><cites>FETCH-LOGICAL-c612t-1cb5553120398184ab6fb24d7850124d8901e9cc78aa8cefd1580b9cbe9ad9783</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC1804380/pdf/$$EPDF$$P50$$Gpubmedcentral$$H</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC1804380/$$EHTML$$P50$$Gpubmedcentral$$H</linktohtml><link.rule.ids>230,314,727,780,784,885,27924,27925,53791,53793</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/17332879$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Wynn, Thomas A</creatorcontrib><title>Common and unique mechanisms regulate fibrosis in various fibroproliferative diseases</title><title>The Journal of clinical investigation</title><addtitle>J Clin Invest</addtitle><description>Fibroproliferative diseases, including the pulmonary fibroses, systemic sclerosis, liver cirrhosis, cardiovascular disease, progressive kidney disease, and macular degeneration, are a leading cause of morbidity and mortality and can affect all tissues and organ systems. Fibrotic tissue remodeling can also influence cancer metastasis and accelerate chronic graft rejection in transplant recipients. Nevertheless, despite its enormous impact on human health, there are currently no approved treatments that directly target the mechanism(s) of fibrosis. The primary goals of this Review series on fibrotic diseases are to discuss some of the major fibroproliferative diseases and to identify the common and unique mechanisms of fibrogenesis that might be exploited in the development of effective antifibrotic therapies.</description><subject>Analysis</subject><subject>Angiotensin II - physiology</subject><subject>Biomedical research</subject><subject>Blood vessels</subject><subject>Bone marrow</subject><subject>Cardiovascular diseases</subject><subject>Cell Proliferation</subject><subject>Chemokines</subject><subject>Chronic Disease</subject><subject>Collagen</subject><subject>Connective tissue</subject><subject>Cytokines</subject><subject>Disease</subject><subject>Embryonic Stem Cells - transplantation</subject><subject>Fibroblasts</subject><subject>Fibroblasts - pathology</subject><subject>Fibroblasts - physiology</subject><subject>Fibrosis</subject><subject>Fibrosis - etiology</subject><subject>Fibrosis - immunology</subject><subject>Fibrosis - therapy</subject><subject>Growth factors</subject><subject>Humans</subject><subject>Infection - immunology</subject><subject>Inflammation</subject><subject>Kidney diseases</subject><subject>Leukocytes</subject><subject>Liver cirrhosis</subject><subject>Macular degeneration</subject><subject>Morbidity</subject><subject>Mortality</subject><subject>Neovascularization, Pathologic - immunology</subject><subject>Neovascularization, Pathologic - metabolism</subject><subject>Neutrophils</subject><subject>Pulmonary fibrosis</subject><subject>Review Series</subject><subject>Scleroderma</subject><subject>Scleroderma (Disease)</subject><subject>Systemic scleroderma</subject><subject>Transforming Growth Factor beta1 - physiology</subject><subject>Wound Healing</subject><issn>0021-9738</issn><issn>1558-8238</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2007</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNqNkl-L1DAUxYMo7jgKfgIpPiz60DV_miZ9EZbB1ZGFBXV9DWl628mSJmPSDvrtzTqj7sg-SB4u3PzuCefmIPSc4DNCBH3zcbVmpJLiAVoQzmUpKZMP0QJjSspGMHmCnqR0gzGpKl49RidEMEalaBboehXGMfhC-66Yvf02QzGC2Whv05iKCMPs9ARFb9sYkk2F9cVORxvmtO9tY3C2h6gnu4Oiswl0gvQUPeq1S_DsUJfo-uLdl9WH8vLq_Xp1flmamtCpJKblnDNCMWskkZVu676lVSckxyRX2WACjTFCai0N9B3hEreNaaHRXSMkW6K3e93t3I7QGfBT1E5tox11_KGCtur4xtuNGsJOEYkrJnEWOD0IxJC9p0mNNhlwTnvIHpXAlNYis0v08h_wJszRZ3OKYsypoDXPULmHBu1AWd-H_KgZwOf9uOCht7l9TmrMGyp_8Wf38Pl0MFpz78Dro4HMTPB9GvScklp__vT_7NXXY_b0DrsB7aZNCm6ebPDpGHy1B02OQ4rQ_9k1weo2iup3FDP64u7f_AUP2WM_AVaM1vw</recordid><startdate>200703</startdate><enddate>200703</enddate><creator>Wynn, Thomas A</creator><general>American Society for Clinical Investigation</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>IOV</scope><scope>ISR</scope><scope>3V.</scope><scope>7RV</scope><scope>7X7</scope><scope>7XB</scope><scope>88A</scope><scope>88E</scope><scope>8AO</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BEC</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>KB0</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M7P</scope><scope>NAPCQ</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>S0X</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>200703</creationdate><title>Common and unique mechanisms regulate fibrosis in various fibroproliferative diseases</title><author>Wynn, Thomas A</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c612t-1cb5553120398184ab6fb24d7850124d8901e9cc78aa8cefd1580b9cbe9ad9783</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2007</creationdate><topic>Analysis</topic><topic>Angiotensin II - 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Fibrotic tissue remodeling can also influence cancer metastasis and accelerate chronic graft rejection in transplant recipients. Nevertheless, despite its enormous impact on human health, there are currently no approved treatments that directly target the mechanism(s) of fibrosis. The primary goals of this Review series on fibrotic diseases are to discuss some of the major fibroproliferative diseases and to identify the common and unique mechanisms of fibrogenesis that might be exploited in the development of effective antifibrotic therapies.</abstract><cop>United States</cop><pub>American Society for Clinical Investigation</pub><pmid>17332879</pmid><doi>10.1172/JCI31487</doi><tpages>6</tpages><oa>free_for_read</oa></addata></record> |
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| source | MEDLINE; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; PubMed Central; Alma/SFX Local Collection |
| subjects | Analysis Angiotensin II - physiology Biomedical research Blood vessels Bone marrow Cardiovascular diseases Cell Proliferation Chemokines Chronic Disease Collagen Connective tissue Cytokines Disease Embryonic Stem Cells - transplantation Fibroblasts Fibroblasts - pathology Fibroblasts - physiology Fibrosis Fibrosis - etiology Fibrosis - immunology Fibrosis - therapy Growth factors Humans Infection - immunology Inflammation Kidney diseases Leukocytes Liver cirrhosis Macular degeneration Morbidity Mortality Neovascularization, Pathologic - immunology Neovascularization, Pathologic - metabolism Neutrophils Pulmonary fibrosis Review Series Scleroderma Scleroderma (Disease) Systemic scleroderma Transforming Growth Factor beta1 - physiology Wound Healing |
| title | Common and unique mechanisms regulate fibrosis in various fibroproliferative diseases |
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