Caveolin-1 as a critical component in the pathogenesis of lung fibrosis of different etiology: Evidences and mechanisms
Caveolin is a structural protein of flask-shaped invaginations of the plasma membrane termed as caveolae and is widely expressed on the endothelial cells, smooth muscle cells and fibroblasts in the different parts of the body including the lung tissues. The expression of caveolin-1 in the lung tissu...
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| Veröffentlicht in: | Experimental and molecular pathology 2019-12, Vol.111, p.104315-104315, Article 104315 |
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| container_title | Experimental and molecular pathology |
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| creator | Kulshrestha, Ritu Singh, Himani Pandey, Apoorva Mehta, Aastha Bhardwaj, Shilpi Jaggi, Amteshwar Singh |
| description | Caveolin is a structural protein of flask-shaped invaginations of the plasma membrane termed as caveolae and is widely expressed on the endothelial cells, smooth muscle cells and fibroblasts in the different parts of the body including the lung tissues. The expression of caveolin-1 in the lung tissues is important to prevent the fibrogenic actions of TGF-β1 in lung fibrosis of different etiology including idiopathic pulmonary fibrosis, systemic sclerosis-associated interstitial lung disease and allergen-induced airway remodeling. Caveolin-1-mediated internalization and degradation of TGF-β1 receptors may possibly account for the decreased actions of TGF-β1. Studies have shown that the deficiency of caveolin-1 is very important in inducing lung fibrosis and its upregulation is reported to prevent lung fibrosis. The biological actions of caveolin-1 involve signaling pathways including JNK signaling, IL-4, STAT-3, miR199a-5p, CXCR4+ and CXCL12. The present review discusses the key role of caveolin and associated signaling pathways in the pathogenesis of lung fibrosis of different etiology. |
| doi_str_mv | 10.1016/j.yexmp.2019.104315 |
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The expression of caveolin-1 in the lung tissues is important to prevent the fibrogenic actions of TGF-β1 in lung fibrosis of different etiology including idiopathic pulmonary fibrosis, systemic sclerosis-associated interstitial lung disease and allergen-induced airway remodeling. Caveolin-1-mediated internalization and degradation of TGF-β1 receptors may possibly account for the decreased actions of TGF-β1. Studies have shown that the deficiency of caveolin-1 is very important in inducing lung fibrosis and its upregulation is reported to prevent lung fibrosis. The biological actions of caveolin-1 involve signaling pathways including JNK signaling, IL-4, STAT-3, miR199a-5p, CXCR4+ and CXCL12. The present review discusses the key role of caveolin and associated signaling pathways in the pathogenesis of lung fibrosis of different etiology.</description><identifier>ISSN: 0014-4800</identifier><identifier>EISSN: 1096-0945</identifier><identifier>DOI: 10.1016/j.yexmp.2019.104315</identifier><identifier>PMID: 31629729</identifier><language>eng</language><publisher>Netherlands: Elsevier Inc</publisher><subject>Airway Remodeling - physiology ; Animals ; Bleomycin ; Caveolin 1 - physiology ; Caveolin-1 ; Cytokines - metabolism ; Epigenesis, Genetic ; Fibrosis ; Humans ; Idiopathic Pulmonary Fibrosis - etiology ; Idiopathic Pulmonary Fibrosis - pathology ; JNK Mitogen-Activated Protein Kinases - metabolism ; Lungs ; Pulmonary Fibrosis - etiology ; Pulmonary Fibrosis - pathology ; Signal Transduction ; STAT Transcription Factors - metabolism ; Transforming growth factor</subject><ispartof>Experimental and molecular pathology, 2019-12, Vol.111, p.104315-104315, Article 104315</ispartof><rights>2019 Elsevier Inc.</rights><rights>Copyright © 2019 Elsevier Inc. All rights reserved.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c359t-9388969cfc79d91fb3cd79f5baea2940cd7f4e99cff40e514ca9d69e3b6b2ec43</citedby><cites>FETCH-LOGICAL-c359t-9388969cfc79d91fb3cd79f5baea2940cd7f4e99cff40e514ca9d69e3b6b2ec43</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/j.yexmp.2019.104315$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,780,784,3550,27924,27925,45995</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/31629729$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Kulshrestha, Ritu</creatorcontrib><creatorcontrib>Singh, Himani</creatorcontrib><creatorcontrib>Pandey, Apoorva</creatorcontrib><creatorcontrib>Mehta, Aastha</creatorcontrib><creatorcontrib>Bhardwaj, Shilpi</creatorcontrib><creatorcontrib>Jaggi, Amteshwar Singh</creatorcontrib><title>Caveolin-1 as a critical component in the pathogenesis of lung fibrosis of different etiology: Evidences and mechanisms</title><title>Experimental and molecular pathology</title><addtitle>Exp Mol Pathol</addtitle><description>Caveolin is a structural protein of flask-shaped invaginations of the plasma membrane termed as caveolae and is widely expressed on the endothelial cells, smooth muscle cells and fibroblasts in the different parts of the body including the lung tissues. The expression of caveolin-1 in the lung tissues is important to prevent the fibrogenic actions of TGF-β1 in lung fibrosis of different etiology including idiopathic pulmonary fibrosis, systemic sclerosis-associated interstitial lung disease and allergen-induced airway remodeling. Caveolin-1-mediated internalization and degradation of TGF-β1 receptors may possibly account for the decreased actions of TGF-β1. Studies have shown that the deficiency of caveolin-1 is very important in inducing lung fibrosis and its upregulation is reported to prevent lung fibrosis. The biological actions of caveolin-1 involve signaling pathways including JNK signaling, IL-4, STAT-3, miR199a-5p, CXCR4+ and CXCL12. The present review discusses the key role of caveolin and associated signaling pathways in the pathogenesis of lung fibrosis of different etiology.</description><subject>Airway Remodeling - physiology</subject><subject>Animals</subject><subject>Bleomycin</subject><subject>Caveolin 1 - physiology</subject><subject>Caveolin-1</subject><subject>Cytokines - metabolism</subject><subject>Epigenesis, Genetic</subject><subject>Fibrosis</subject><subject>Humans</subject><subject>Idiopathic Pulmonary Fibrosis - etiology</subject><subject>Idiopathic Pulmonary Fibrosis - pathology</subject><subject>JNK Mitogen-Activated Protein Kinases - metabolism</subject><subject>Lungs</subject><subject>Pulmonary Fibrosis - etiology</subject><subject>Pulmonary Fibrosis - pathology</subject><subject>Signal Transduction</subject><subject>STAT Transcription Factors - metabolism</subject><subject>Transforming growth factor</subject><issn>0014-4800</issn><issn>1096-0945</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2019</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kE1rGzEQhkVpaZy0v6AQdMxlXWmlXXsCOQSTfkCgl_YstNLIltmVNtLaif995drJsSeh4XnnZR5CvnA254y3X7fzA74M47xmHMpECt68IzPOoK0YyOY9mTHGZSWXjF2Qy5y3jDFgvP5ILgRva1jUMCPPK73H2PtQcaoz1dQkP3mje2riMMaAYaI-0GmDdNTTJq4xYPaZRkf7XVhT57sUzwPrncN0TODkYx_Xh1v6sPcWg8GyOlg6oNno4POQP5EPTvcZP5_fK_Ln28Pv1Y_q8df3n6v7x8qIBqYKxHIJLRhnFmCBu04YuwDXdBp1DZKVn5MIBXCSYcOl0WBbQNG1XY1Giityc9o7pvi0wzypwWeDfa8Dxl1WtWALURqWvKDihJpyUU7o1Jj8oNNBcaaOxtVW_TOujsbVyXhJXZ8Ldt2A9i3zqrgAdycAy5l7j0ll449KrE9oJmWj_2_BX_Y5lWQ</recordid><startdate>201912</startdate><enddate>201912</enddate><creator>Kulshrestha, Ritu</creator><creator>Singh, Himani</creator><creator>Pandey, Apoorva</creator><creator>Mehta, Aastha</creator><creator>Bhardwaj, Shilpi</creator><creator>Jaggi, Amteshwar Singh</creator><general>Elsevier 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>7X8</scope></search><sort><creationdate>201912</creationdate><title>Caveolin-1 as a critical component in the pathogenesis of lung fibrosis of different etiology: Evidences and mechanisms</title><author>Kulshrestha, Ritu ; Singh, Himani ; Pandey, Apoorva ; Mehta, Aastha ; Bhardwaj, Shilpi ; Jaggi, Amteshwar Singh</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c359t-9388969cfc79d91fb3cd79f5baea2940cd7f4e99cff40e514ca9d69e3b6b2ec43</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2019</creationdate><topic>Airway Remodeling - physiology</topic><topic>Animals</topic><topic>Bleomycin</topic><topic>Caveolin 1 - physiology</topic><topic>Caveolin-1</topic><topic>Cytokines - metabolism</topic><topic>Epigenesis, Genetic</topic><topic>Fibrosis</topic><topic>Humans</topic><topic>Idiopathic Pulmonary Fibrosis - etiology</topic><topic>Idiopathic Pulmonary Fibrosis - pathology</topic><topic>JNK Mitogen-Activated Protein Kinases - metabolism</topic><topic>Lungs</topic><topic>Pulmonary Fibrosis - etiology</topic><topic>Pulmonary Fibrosis - pathology</topic><topic>Signal Transduction</topic><topic>STAT Transcription Factors - metabolism</topic><topic>Transforming growth factor</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Kulshrestha, Ritu</creatorcontrib><creatorcontrib>Singh, Himani</creatorcontrib><creatorcontrib>Pandey, Apoorva</creatorcontrib><creatorcontrib>Mehta, Aastha</creatorcontrib><creatorcontrib>Bhardwaj, Shilpi</creatorcontrib><creatorcontrib>Jaggi, Amteshwar Singh</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Experimental and molecular pathology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Kulshrestha, Ritu</au><au>Singh, Himani</au><au>Pandey, Apoorva</au><au>Mehta, Aastha</au><au>Bhardwaj, Shilpi</au><au>Jaggi, Amteshwar Singh</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Caveolin-1 as a critical component in the pathogenesis of lung fibrosis of different etiology: Evidences and mechanisms</atitle><jtitle>Experimental and molecular pathology</jtitle><addtitle>Exp Mol Pathol</addtitle><date>2019-12</date><risdate>2019</risdate><volume>111</volume><spage>104315</spage><epage>104315</epage><pages>104315-104315</pages><artnum>104315</artnum><issn>0014-4800</issn><eissn>1096-0945</eissn><abstract>Caveolin is a structural protein of flask-shaped invaginations of the plasma membrane termed as caveolae and is widely expressed on the endothelial cells, smooth muscle cells and fibroblasts in the different parts of the body including the lung tissues. The expression of caveolin-1 in the lung tissues is important to prevent the fibrogenic actions of TGF-β1 in lung fibrosis of different etiology including idiopathic pulmonary fibrosis, systemic sclerosis-associated interstitial lung disease and allergen-induced airway remodeling. Caveolin-1-mediated internalization and degradation of TGF-β1 receptors may possibly account for the decreased actions of TGF-β1. Studies have shown that the deficiency of caveolin-1 is very important in inducing lung fibrosis and its upregulation is reported to prevent lung fibrosis. The biological actions of caveolin-1 involve signaling pathways including JNK signaling, IL-4, STAT-3, miR199a-5p, CXCR4+ and CXCL12. 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| subjects | Airway Remodeling - physiology Animals Bleomycin Caveolin 1 - physiology Caveolin-1 Cytokines - metabolism Epigenesis, Genetic Fibrosis Humans Idiopathic Pulmonary Fibrosis - etiology Idiopathic Pulmonary Fibrosis - pathology JNK Mitogen-Activated Protein Kinases - metabolism Lungs Pulmonary Fibrosis - etiology Pulmonary Fibrosis - pathology Signal Transduction STAT Transcription Factors - metabolism Transforming growth factor |
| title | Caveolin-1 as a critical component in the pathogenesis of lung fibrosis of different etiology: Evidences and mechanisms |
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