The TGFβ superfamily in cardiac dysfunction
Abstract TGFβ superfamily includes the transforming growth factor βs (TGFβs), bone morphogenetic proteins (BMPs), growth and differentiation factors (GDFs) and Activin/Inhibin families of ligands. Among the 33 members of TGFβ superfamily ligands, many act on multiple types of cells within the heart,...
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Veröffentlicht in: | Acta biochimica et biophysica Sinica 2018-04, Vol.50 (4), p.323-335 |
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creator | Wu, Jian Jackson-Weaver, Olan Xu, Jian |
description | Abstract
TGFβ superfamily includes the transforming growth factor βs (TGFβs), bone morphogenetic proteins (BMPs), growth and differentiation factors (GDFs) and Activin/Inhibin families of ligands. Among the 33 members of TGFβ superfamily ligands, many act on multiple types of cells within the heart, including cardiomyocytes, cardiac fibroblasts/myofibroblasts, coronary endothelial cells, smooth muscle cells, and immune cells (e.g. monocytes/macrophages and neutrophils). In this review, we highlight recent discoveries on TGFβs, BMPs, and GDFs in different cardiac residential cellular components, in association with functional impacts in heart development, injury repair, and dysfunction. Specifically, we will review the roles of TGFβs, BMPs, and GDFs in cardiac hypertrophy, fibrosis, contractility, metabolism, angiogenesis, and regeneration. |
doi_str_mv | 10.1093/abbs/gmy007 |
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TGFβ superfamily includes the transforming growth factor βs (TGFβs), bone morphogenetic proteins (BMPs), growth and differentiation factors (GDFs) and Activin/Inhibin families of ligands. Among the 33 members of TGFβ superfamily ligands, many act on multiple types of cells within the heart, including cardiomyocytes, cardiac fibroblasts/myofibroblasts, coronary endothelial cells, smooth muscle cells, and immune cells (e.g. monocytes/macrophages and neutrophils). In this review, we highlight recent discoveries on TGFβs, BMPs, and GDFs in different cardiac residential cellular components, in association with functional impacts in heart development, injury repair, and dysfunction. Specifically, we will review the roles of TGFβs, BMPs, and GDFs in cardiac hypertrophy, fibrosis, contractility, metabolism, angiogenesis, and regeneration.</description><identifier>ISSN: 1672-9145</identifier><identifier>EISSN: 1745-7270</identifier><identifier>DOI: 10.1093/abbs/gmy007</identifier><identifier>PMID: 29462261</identifier><language>eng</language><publisher>China: Oxford University Press</publisher><subject>Animals ; Bone Morphogenetic Proteins - metabolism ; Cell Survival ; Editor's Choice ; Fibroblasts - metabolism ; Growth Differentiation Factors - metabolism ; Heart Diseases - metabolism ; Humans ; Hypertrophy ; Ligands ; Mice ; Mice, Knockout ; Myocytes, Cardiac - metabolism ; Regeneration ; Review ; Signal Transduction ; Transforming Growth Factor beta - physiology</subject><ispartof>Acta biochimica et biophysica Sinica, 2018-04, Vol.50 (4), p.323-335</ispartof><rights>The Author(s) 2018. Published by Oxford University Press on behalf of the Institute of Biochemistry and Cell Biology, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences. All rights reserved. For permissions, please e-mail: journals.permissions@oup.com 2018</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c375t-685fb58f3a390e1570a98e3f2bfeecf770cf0a7dfc4f6cb1f9172e54c8bc9d373</citedby><cites>FETCH-LOGICAL-c375t-685fb58f3a390e1570a98e3f2bfeecf770cf0a7dfc4f6cb1f9172e54c8bc9d373</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/PMC6676786/pdf/$$EPDF$$P50$$Gpubmedcentral$$H</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC6676786/$$EHTML$$P50$$Gpubmedcentral$$H</linktohtml><link.rule.ids>230,314,723,776,780,881,27901,27902,53766,53768</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/29462261$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Wu, Jian</creatorcontrib><creatorcontrib>Jackson-Weaver, Olan</creatorcontrib><creatorcontrib>Xu, Jian</creatorcontrib><title>The TGFβ superfamily in cardiac dysfunction</title><title>Acta biochimica et biophysica Sinica</title><addtitle>Acta Biochim Biophys Sin (Shanghai)</addtitle><description>Abstract
TGFβ superfamily includes the transforming growth factor βs (TGFβs), bone morphogenetic proteins (BMPs), growth and differentiation factors (GDFs) and Activin/Inhibin families of ligands. Among the 33 members of TGFβ superfamily ligands, many act on multiple types of cells within the heart, including cardiomyocytes, cardiac fibroblasts/myofibroblasts, coronary endothelial cells, smooth muscle cells, and immune cells (e.g. monocytes/macrophages and neutrophils). In this review, we highlight recent discoveries on TGFβs, BMPs, and GDFs in different cardiac residential cellular components, in association with functional impacts in heart development, injury repair, and dysfunction. Specifically, we will review the roles of TGFβs, BMPs, and GDFs in cardiac hypertrophy, fibrosis, contractility, metabolism, angiogenesis, and regeneration.</description><subject>Animals</subject><subject>Bone Morphogenetic Proteins - metabolism</subject><subject>Cell Survival</subject><subject>Editor's Choice</subject><subject>Fibroblasts - metabolism</subject><subject>Growth Differentiation Factors - metabolism</subject><subject>Heart Diseases - metabolism</subject><subject>Humans</subject><subject>Hypertrophy</subject><subject>Ligands</subject><subject>Mice</subject><subject>Mice, Knockout</subject><subject>Myocytes, Cardiac - metabolism</subject><subject>Regeneration</subject><subject>Review</subject><subject>Signal Transduction</subject><subject>Transforming Growth Factor beta - physiology</subject><issn>1672-9145</issn><issn>1745-7270</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2018</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kE1LwzAYgIMobk5P3qUnEbQuH03SXgQZbgoDL_Mc0jTZIv0yaQf9W_4Qf5MdnUMvnvJCHp735QHgEsF7BBMylWnqp-uig5AfgTHiEQ055vC4nxnHYYIiOgJn3r9DSBhD8BSMcBIxjBkag7vVRgerxfzrM_BtrZ2Rhc27wJaBki6zUgVZ501bqsZW5Tk4MTL3-mL_TsDb_Gk1ew6Xr4uX2eMyVITTJmQxNSmNDZEkgRpRDmUSa2JwarRWhnOoDJQ8MyoyTKXIJIhjTSMVpyrJCCcT8DB46zYtdKZ02TiZi9rZQrpOVNKKvz-l3Yh1tRWMccZj1gtu9gJXfbTaN6KwXuk8l6WuWi9w3wohGtMdejugylXeO20OaxAUu75i11cMfXv66vdlB_YnaA9cD0DV1v-avgGGOYY2</recordid><startdate>20180401</startdate><enddate>20180401</enddate><creator>Wu, Jian</creator><creator>Jackson-Weaver, Olan</creator><creator>Xu, Jian</creator><general>Oxford University Press</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>20180401</creationdate><title>The TGFβ superfamily in cardiac dysfunction</title><author>Wu, Jian ; Jackson-Weaver, Olan ; Xu, Jian</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c375t-685fb58f3a390e1570a98e3f2bfeecf770cf0a7dfc4f6cb1f9172e54c8bc9d373</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2018</creationdate><topic>Animals</topic><topic>Bone Morphogenetic Proteins - metabolism</topic><topic>Cell Survival</topic><topic>Editor's Choice</topic><topic>Fibroblasts - metabolism</topic><topic>Growth Differentiation Factors - metabolism</topic><topic>Heart Diseases - metabolism</topic><topic>Humans</topic><topic>Hypertrophy</topic><topic>Ligands</topic><topic>Mice</topic><topic>Mice, Knockout</topic><topic>Myocytes, Cardiac - metabolism</topic><topic>Regeneration</topic><topic>Review</topic><topic>Signal Transduction</topic><topic>Transforming Growth Factor beta - physiology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Wu, Jian</creatorcontrib><creatorcontrib>Jackson-Weaver, Olan</creatorcontrib><creatorcontrib>Xu, Jian</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>Acta biochimica et biophysica Sinica</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Wu, Jian</au><au>Jackson-Weaver, Olan</au><au>Xu, Jian</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>The TGFβ superfamily in cardiac dysfunction</atitle><jtitle>Acta biochimica et biophysica Sinica</jtitle><addtitle>Acta Biochim Biophys Sin (Shanghai)</addtitle><date>2018-04-01</date><risdate>2018</risdate><volume>50</volume><issue>4</issue><spage>323</spage><epage>335</epage><pages>323-335</pages><issn>1672-9145</issn><eissn>1745-7270</eissn><abstract>Abstract
TGFβ superfamily includes the transforming growth factor βs (TGFβs), bone morphogenetic proteins (BMPs), growth and differentiation factors (GDFs) and Activin/Inhibin families of ligands. Among the 33 members of TGFβ superfamily ligands, many act on multiple types of cells within the heart, including cardiomyocytes, cardiac fibroblasts/myofibroblasts, coronary endothelial cells, smooth muscle cells, and immune cells (e.g. monocytes/macrophages and neutrophils). In this review, we highlight recent discoveries on TGFβs, BMPs, and GDFs in different cardiac residential cellular components, in association with functional impacts in heart development, injury repair, and dysfunction. Specifically, we will review the roles of TGFβs, BMPs, and GDFs in cardiac hypertrophy, fibrosis, contractility, metabolism, angiogenesis, and regeneration.</abstract><cop>China</cop><pub>Oxford University Press</pub><pmid>29462261</pmid><doi>10.1093/abbs/gmy007</doi><tpages>13</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 | Animals Bone Morphogenetic Proteins - metabolism Cell Survival Editor's Choice Fibroblasts - metabolism Growth Differentiation Factors - metabolism Heart Diseases - metabolism Humans Hypertrophy Ligands Mice Mice, Knockout Myocytes, Cardiac - metabolism Regeneration Review Signal Transduction Transforming Growth Factor beta - physiology |
title | The TGFβ superfamily in cardiac dysfunction |
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