Role of inflammatory cells in fibroblast activation
Abstract Although fibrosis is an essential response to acute cardiac tissue injury, prolonged myofibroblast activation and progressive fibrosis lead to further distortion of tissue architecture and worsened cardiac function. Thus, optimal tissue repair following injury requires tight control over my...
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Veröffentlicht in: | Journal of molecular and cellular cardiology 2016-04, Vol.93, p.143-148 |
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description | Abstract Although fibrosis is an essential response to acute cardiac tissue injury, prolonged myofibroblast activation and progressive fibrosis lead to further distortion of tissue architecture and worsened cardiac function. Thus, optimal tissue repair following injury requires tight control over myofibroblast activation. It is now recognized that inflammation plays a critical role in regulating fibrosis. In this review we will highlight how advances in the field of innate immunity have led to a better understanding of the role of inflammation in cardiovascular disease and, in particular, in the regulation of fibrosis. Specifically, we will discuss how the innate immune system recognizes tissue damage in settings of acute injury and chronic cardiovascular disease. We will also review the role of different cell populations in this response, particularly the unique role of different macrophage subsets and mast cells. |
doi_str_mv | 10.1016/j.yjmcc.2015.11.016 |
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Thus, optimal tissue repair following injury requires tight control over myofibroblast activation. It is now recognized that inflammation plays a critical role in regulating fibrosis. In this review we will highlight how advances in the field of innate immunity have led to a better understanding of the role of inflammation in cardiovascular disease and, in particular, in the regulation of fibrosis. Specifically, we will discuss how the innate immune system recognizes tissue damage in settings of acute injury and chronic cardiovascular disease. 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Thus, optimal tissue repair following injury requires tight control over myofibroblast activation. It is now recognized that inflammation plays a critical role in regulating fibrosis. In this review we will highlight how advances in the field of innate immunity have led to a better understanding of the role of inflammation in cardiovascular disease and, in particular, in the regulation of fibrosis. Specifically, we will discuss how the innate immune system recognizes tissue damage in settings of acute injury and chronic cardiovascular disease. We will also review the role of different cell populations in this response, particularly the unique role of different macrophage subsets and mast cells.</description><subject>Animals</subject><subject>Cardiovascular</subject><subject>Fibroblasts - metabolism</subject><subject>Fibrosis</subject><subject>Humans</subject><subject>Immune System - cytology</subject><subject>Immune System - immunology</subject><subject>Immune System - metabolism</subject><subject>Immunity, Innate</subject><subject>Inflammation</subject><subject>Inflammation - etiology</subject><subject>Inflammation - metabolism</subject><subject>Inflammation - pathology</subject><subject>Innate immunity</subject><subject>Macrophage</subject><subject>Mast cell</subject><subject>Myocarditis - etiology</subject><subject>Myocarditis - metabolism</subject><subject>Myocarditis - pathology</subject><subject>Myocarditis - physiopathology</subject><subject>Myocardium - metabolism</subject><subject>Myocardium - pathology</subject><subject>Myofibroblasts - metabolism</subject><subject>Signal Transduction</subject><issn>0022-2828</issn><issn>1095-8584</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2016</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFUU2L1TAUDaI4z9FfIEiXblrz2aQLB2QYP2BA8APcXZL0VlPbZkz6Hrx_b-obB3XjKnDuOefenEPIU0YbRln7YmyO4-x9wylTDWNNwe6RHaOdqo0y8j7ZUcp5zQ03Z-RRziOltJNCPCRnvFWd0FzsiPgQJ6ziUIVlmOw82zWmY-VxmnKBqiG4FN1k81pZv4aDXUNcHpMHg50yPrl9z8nn11efLt_W1-_fvLt8dV17Zehaa4dSU6vRIDV2aD0ya9ygZd-j89zynktdxtq5TnnlOq6pkkY5hdJ4tOKcXJx8b_Zuxt7jsiY7wU0Ks01HiDbA35MlfIOv8QDSyFYxVgye3xqk-GOPeYU55O1vdsG4z8C0kbpsNG2hihPVp5hzwuFuDaOwxQ0j_IobtriBMShYUT3788I7ze98C-HliYAlp0PABNkHXDz2IaFfoY_hPwsu_tH7KSzB2-k7HjGPcZ-WUgEwyBwofNwa3wpnSlDG-RfxE8KRqKU</recordid><startdate>20160401</startdate><enddate>20160401</enddate><creator>Hartupee, Justin</creator><creator>Mann, Douglas L</creator><general>Elsevier Ltd</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><scope>5PM</scope><orcidid>https://orcid.org/0000-0002-2516-0145</orcidid></search><sort><creationdate>20160401</creationdate><title>Role of inflammatory cells in fibroblast activation</title><author>Hartupee, Justin ; Mann, Douglas L</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c580t-7be470a7e8e08af6ce1a8bf74ddebc2a2d247a7e7bb95c5b92705485b5e48cea3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2016</creationdate><topic>Animals</topic><topic>Cardiovascular</topic><topic>Fibroblasts - metabolism</topic><topic>Fibrosis</topic><topic>Humans</topic><topic>Immune System - cytology</topic><topic>Immune System - immunology</topic><topic>Immune System - metabolism</topic><topic>Immunity, Innate</topic><topic>Inflammation</topic><topic>Inflammation - etiology</topic><topic>Inflammation - metabolism</topic><topic>Inflammation - pathology</topic><topic>Innate immunity</topic><topic>Macrophage</topic><topic>Mast cell</topic><topic>Myocarditis - etiology</topic><topic>Myocarditis - metabolism</topic><topic>Myocarditis - pathology</topic><topic>Myocarditis - physiopathology</topic><topic>Myocardium - metabolism</topic><topic>Myocardium - pathology</topic><topic>Myofibroblasts - metabolism</topic><topic>Signal Transduction</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Hartupee, Justin</creatorcontrib><creatorcontrib>Mann, Douglas L</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><collection>PubMed Central (Full Participant titles)</collection><jtitle>Journal of molecular and cellular cardiology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Hartupee, Justin</au><au>Mann, Douglas L</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Role of inflammatory cells in fibroblast activation</atitle><jtitle>Journal of molecular and cellular cardiology</jtitle><addtitle>J Mol Cell Cardiol</addtitle><date>2016-04-01</date><risdate>2016</risdate><volume>93</volume><spage>143</spage><epage>148</epage><pages>143-148</pages><issn>0022-2828</issn><eissn>1095-8584</eissn><abstract>Abstract Although fibrosis is an essential response to acute cardiac tissue injury, prolonged myofibroblast activation and progressive fibrosis lead to further distortion of tissue architecture and worsened cardiac function. 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subjects | Animals Cardiovascular Fibroblasts - metabolism Fibrosis Humans Immune System - cytology Immune System - immunology Immune System - metabolism Immunity, Innate Inflammation Inflammation - etiology Inflammation - metabolism Inflammation - pathology Innate immunity Macrophage Mast cell Myocarditis - etiology Myocarditis - metabolism Myocarditis - pathology Myocarditis - physiopathology Myocardium - metabolism Myocardium - pathology Myofibroblasts - metabolism Signal Transduction |
title | Role of inflammatory cells in fibroblast activation |
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