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Oncostatin M and its role in fibrosis
Oncostain M, a member of the IL-6 family of cytokines, is produced by immune cells in response to infections and tissue injury. OSM has a broad, often context-dependent effect on various cellular processes including differentiation, hematopoiesis, cell proliferation, and cell survival. OSM signaling...
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Published in: | Connective tissue research 2019-01, Vol.60 (1), p.40-49 |
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creator | Stawski, Lukasz Trojanowska, Maria |
description | Oncostain M, a member of the IL-6 family of cytokines, is produced by immune cells in response to infections and tissue injury. OSM has a broad, often context-dependent effect on various cellular processes including differentiation, hematopoiesis, cell proliferation, and cell survival. OSM signaling is initiated by binding to type I (LIFRβ/gp130) or type II (OSMRβ/gp130) receptor complexes and involves activation of Janus kinase/signal transducer and activator of transcription, mitogen-activated protein kinase, and phosphatidylinositol-3-kinase. High levels of OSM have been detected in many chronic inflammatory conditions characterized by fibrosis, giving a rationale to target OSM for the treatment of these diseases. Here we discuss the current knowledge on the role of OSM in various stages of the fibrotic process including inflammation, vascular dysfunction, and activation of fibroblasts. |
doi_str_mv | 10.1080/03008207.2018.1500558 |
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Here we discuss the current knowledge on the role of OSM in various stages of the fibrotic process including inflammation, vascular dysfunction, and activation of fibroblasts.</description><subject>Animals</subject><subject>ECM</subject><subject>Fibrosis</subject><subject>Humans</subject><subject>inflammation</subject><subject>Inflammation - pathology</subject><subject>Models, Biological</subject><subject>Oncostatin M - metabolism</subject><subject>OSM</subject><subject>Signal Transduction</subject><subject>vascular injury</subject><subject>Vascular System Injuries - metabolism</subject><subject>Vascular System Injuries - pathology</subject><issn>0300-8207</issn><issn>1607-8438</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2019</creationdate><recordtype>article</recordtype><recordid>eNp9kE1LxDAQhoMo7vrxE5ReBC9dJ02TJhdRFr9gZS96DmmbaqRN1qSr7L83ZT_Qi6fA5Jl3Zh6EzjBMMHC4AgLAMygmGWA-wRSAUr6HxphBkfKc8H00Hph0gEboKIQPAExIRg_RKNYpK5gYo4u5rVzoVW9s8pwoWyemD4l3rU5ipTGld8GEE3TQqDbo0817jF7v716mj-ls_vA0vZ2lVc54n5YKU8xIpmiB87rJhNZVgTPRlLhQeSEqxnjNBInDhcqZoCA00yAEqQXjeU2O0fU6d7EsO11X2vZetXLhTaf8Sjpl5N8fa97lm_uSjOQiwyIGXG4CvPtc6tDLzoRKt62y2i2DjC6EiLtiHlG6Rqt4YvC62Y3BIAfFcqtYDorlRnHsO_-9465r6zQCN2vA2Mb5Tn0739ayV6vW-cYrW5kgyf8zfgAFMYkG</recordid><startdate>20190102</startdate><enddate>20190102</enddate><creator>Stawski, Lukasz</creator><creator>Trojanowska, Maria</creator><general>Taylor & Francis</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></search><sort><creationdate>20190102</creationdate><title>Oncostatin M and its role in fibrosis</title><author>Stawski, Lukasz ; Trojanowska, Maria</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c468t-ba151632a5714df29eec7129fb17a479c668d6930569a469509e6e0993d9684d3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2019</creationdate><topic>Animals</topic><topic>ECM</topic><topic>Fibrosis</topic><topic>Humans</topic><topic>inflammation</topic><topic>Inflammation - pathology</topic><topic>Models, Biological</topic><topic>Oncostatin M - metabolism</topic><topic>OSM</topic><topic>Signal Transduction</topic><topic>vascular injury</topic><topic>Vascular System Injuries - metabolism</topic><topic>Vascular System Injuries - pathology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Stawski, Lukasz</creatorcontrib><creatorcontrib>Trojanowska, Maria</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>Connective tissue research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Stawski, Lukasz</au><au>Trojanowska, Maria</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Oncostatin M and its role in fibrosis</atitle><jtitle>Connective tissue research</jtitle><addtitle>Connect Tissue Res</addtitle><date>2019-01-02</date><risdate>2019</risdate><volume>60</volume><issue>1</issue><spage>40</spage><epage>49</epage><pages>40-49</pages><issn>0300-8207</issn><eissn>1607-8438</eissn><abstract>Oncostain M, a member of the IL-6 family of cytokines, is produced by immune cells in response to infections and tissue injury. 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subjects | Animals ECM Fibrosis Humans inflammation Inflammation - pathology Models, Biological Oncostatin M - metabolism OSM Signal Transduction vascular injury Vascular System Injuries - metabolism Vascular System Injuries - pathology |
title | Oncostatin M and its role in fibrosis |
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