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Intercalated discs: cellular adhesion and signaling in heart health and diseases
Intercalated discs (ICDs) are highly orchestrated structures that connect neighboring cardiomyocytes in the heart. Three major complexes are distinguished in ICD: desmosome, adherens junction (AJ), and gap junction (GJ). Desmosomes are major cell adhesion junctions that anchor cell membrane to the i...
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Published in: | Heart failure reviews 2019, Vol.24 (1), p.115-132 |
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description | Intercalated discs (ICDs) are highly orchestrated structures that connect neighboring cardiomyocytes in the heart. Three major complexes are distinguished in ICD: desmosome, adherens junction (AJ), and gap junction (GJ). Desmosomes are major cell adhesion junctions that anchor cell membrane to the intermediate filament network; AJs connect the actin cytoskeleton of adjacent cells; and gap junctions metabolically and electrically connect the cytoplasm of adjacent cardiomyocytes. All these complexes work as a single unit, the so-called area composita, interdependently rather than individually. Mutation or altered expression of ICD proteins results in various cardiac diseases, such as ARVC (arrhythmogenic right ventricular cardiomyopathy), dilated cardiomyopathy, and hypotrophy cardiomyopathy, eventually leading to heart failure. In this article, we first review the recent findings on the structural organization of ICD and their functions and then focus on the recent advances in molecular pathogenesis of the ICD-related heart diseases, which include two major areas: i) the ICD gene mutations in cardiac diseases, and ii) the involvement of ICD proteins in signal transduction pathways leading to myocardium remodeling and eventual heart failure. These major ICD-related signaling pathways include Wnt/β-catenin pathway, p38 MAPK cascade, Rho-dependent serum response factor (SRF) signaling, calcineurin/NFAT signaling, Hippo kinase cascade, etc., which are differentially regulated in pathological conditions. |
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Three major complexes are distinguished in ICD: desmosome, adherens junction (AJ), and gap junction (GJ). Desmosomes are major cell adhesion junctions that anchor cell membrane to the intermediate filament network; AJs connect the actin cytoskeleton of adjacent cells; and gap junctions metabolically and electrically connect the cytoplasm of adjacent cardiomyocytes. All these complexes work as a single unit, the so-called area composita, interdependently rather than individually. Mutation or altered expression of ICD proteins results in various cardiac diseases, such as ARVC (arrhythmogenic right ventricular cardiomyopathy), dilated cardiomyopathy, and hypotrophy cardiomyopathy, eventually leading to heart failure. In this article, we first review the recent findings on the structural organization of ICD and their functions and then focus on the recent advances in molecular pathogenesis of the ICD-related heart diseases, which include two major areas: i) the ICD gene mutations in cardiac diseases, and ii) the involvement of ICD proteins in signal transduction pathways leading to myocardium remodeling and eventual heart failure. 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All Rights Reserved.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c372t-b4c0360a4c74ce7f08bce4b4ea13511648741f5ba733bd564553341374d775ba3</citedby><cites>FETCH-LOGICAL-c372t-b4c0360a4c74ce7f08bce4b4ea13511648741f5ba733bd564553341374d775ba3</cites><orcidid>0000-0002-3177-0070</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/30288656$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Zhao, Guangze</creatorcontrib><creatorcontrib>Qiu, Ye</creatorcontrib><creatorcontrib>Zhang, Huifang M.</creatorcontrib><creatorcontrib>Yang, Decheng</creatorcontrib><title>Intercalated discs: cellular adhesion and signaling in heart health and diseases</title><title>Heart failure reviews</title><addtitle>Heart Fail Rev</addtitle><addtitle>Heart Fail Rev</addtitle><description>Intercalated discs (ICDs) are highly orchestrated structures that connect neighboring cardiomyocytes in the heart. Three major complexes are distinguished in ICD: desmosome, adherens junction (AJ), and gap junction (GJ). Desmosomes are major cell adhesion junctions that anchor cell membrane to the intermediate filament network; AJs connect the actin cytoskeleton of adjacent cells; and gap junctions metabolically and electrically connect the cytoplasm of adjacent cardiomyocytes. All these complexes work as a single unit, the so-called area composita, interdependently rather than individually. Mutation or altered expression of ICD proteins results in various cardiac diseases, such as ARVC (arrhythmogenic right ventricular cardiomyopathy), dilated cardiomyopathy, and hypotrophy cardiomyopathy, eventually leading to heart failure. In this article, we first review the recent findings on the structural organization of ICD and their functions and then focus on the recent advances in molecular pathogenesis of the ICD-related heart diseases, which include two major areas: i) the ICD gene mutations in cardiac diseases, and ii) the involvement of ICD proteins in signal transduction pathways leading to myocardium remodeling and eventual heart failure. These major ICD-related signaling pathways include Wnt/β-catenin pathway, p38 MAPK cascade, Rho-dependent serum response factor (SRF) signaling, calcineurin/NFAT signaling, Hippo kinase cascade, etc., which are differentially regulated in pathological conditions.</description><subject>Actin</subject><subject>Adherens Junctions - chemistry</subject><subject>Adherens Junctions - genetics</subject><subject>Adherens Junctions - metabolism</subject><subject>Animals</subject><subject>Calcineurin</subject><subject>Cardiology</subject><subject>Cardiomyocytes</subject><subject>Cardiomyopathy</subject><subject>Cell Adhesion</subject><subject>Cell adhesion & migration</subject><subject>Cell membranes</subject><subject>Coronary artery disease</subject><subject>Cytoplasm</subject><subject>Cytoskeleton</subject><subject>Desmosomes</subject><subject>Desmosomes - chemistry</subject><subject>Desmosomes - genetics</subject><subject>Desmosomes - metabolism</subject><subject>Dilated cardiomyopathy</subject><subject>Gap junctions</subject><subject>Gap Junctions - chemistry</subject><subject>Gap Junctions - genetics</subject><subject>Gap Junctions - metabolism</subject><subject>Heart diseases</subject><subject>Heart Diseases - genetics</subject><subject>Heart Diseases - metabolism</subject><subject>Heart failure</subject><subject>Humans</subject><subject>Kinases</subject><subject>MAP kinase</subject><subject>Medicine</subject><subject>Medicine & Public Health</subject><subject>Mutation</subject><subject>Mutation, Missense</subject><subject>Myocardium</subject><subject>Myocardium - metabolism</subject><subject>Myocytes, Cardiac - metabolism</subject><subject>NF-AT protein</subject><subject>Serum response factor</subject><subject>Signal Transduction</subject><subject>Ventricle</subject><subject>Wnt protein</subject><subject>β-Catenin</subject><issn>1382-4147</issn><issn>1573-7322</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2019</creationdate><recordtype>article</recordtype><recordid>eNp1kMtOwzAQRS0EoqXwAWxQJDZsAn6M45QdqnhUqgQLWFuOM2lTpU6xkwV_j0sKSEhs7JHn3OuZS8g5o9eMUnUTGFXAUsrydKpApOqAjJlUsRCcH8Za5DwFBmpETkJYU0phCvSYjATleZ7JbExe5q5Db01jOiyTsg423CYWm6ZvjE9MucJQty4xrkxCvXSmqd0yqV2yQuO73dl0q69ulKIJGE7JUWWagGf7e0LeHu5fZ0_p4vlxPrtbpFYo3qUFWCoyasAqsKgqmhcWoQA0TEjGMsjjZpUsjBKiKGUGUgoBTCgolYrPYkKuBt-tb997DJ3exOHj4MZh2wfNo0kuuRQ8opd_0HXb-7jLQHE5ZYJFig2U9W0IHiu99fXG-A_NqN7FrYe4dYxb7-LWKmou9s59scHyR_GdbwT4AITYckv0v1__7_oJ11OI0g</recordid><startdate>2019</startdate><enddate>2019</enddate><creator>Zhao, Guangze</creator><creator>Qiu, Ye</creator><creator>Zhang, Huifang M.</creator><creator>Yang, Decheng</creator><general>Springer US</general><general>Springer Nature B.V</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>3V.</scope><scope>7QP</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>8G5</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>GUQSH</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>M2O</scope><scope>MBDVC</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>7X8</scope><orcidid>https://orcid.org/0000-0002-3177-0070</orcidid></search><sort><creationdate>2019</creationdate><title>Intercalated discs: cellular adhesion and signaling in heart health and diseases</title><author>Zhao, Guangze ; Qiu, Ye ; Zhang, Huifang M. ; Yang, Decheng</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c372t-b4c0360a4c74ce7f08bce4b4ea13511648741f5ba733bd564553341374d775ba3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2019</creationdate><topic>Actin</topic><topic>Adherens Junctions - chemistry</topic><topic>Adherens Junctions - genetics</topic><topic>Adherens Junctions - metabolism</topic><topic>Animals</topic><topic>Calcineurin</topic><topic>Cardiology</topic><topic>Cardiomyocytes</topic><topic>Cardiomyopathy</topic><topic>Cell Adhesion</topic><topic>Cell adhesion & migration</topic><topic>Cell membranes</topic><topic>Coronary artery disease</topic><topic>Cytoplasm</topic><topic>Cytoskeleton</topic><topic>Desmosomes</topic><topic>Desmosomes - chemistry</topic><topic>Desmosomes - genetics</topic><topic>Desmosomes - metabolism</topic><topic>Dilated cardiomyopathy</topic><topic>Gap junctions</topic><topic>Gap Junctions - chemistry</topic><topic>Gap Junctions - genetics</topic><topic>Gap Junctions - metabolism</topic><topic>Heart diseases</topic><topic>Heart Diseases - genetics</topic><topic>Heart Diseases - metabolism</topic><topic>Heart failure</topic><topic>Humans</topic><topic>Kinases</topic><topic>MAP kinase</topic><topic>Medicine</topic><topic>Medicine & Public Health</topic><topic>Mutation</topic><topic>Mutation, Missense</topic><topic>Myocardium</topic><topic>Myocardium - metabolism</topic><topic>Myocytes, Cardiac - metabolism</topic><topic>NF-AT protein</topic><topic>Serum response factor</topic><topic>Signal Transduction</topic><topic>Ventricle</topic><topic>Wnt protein</topic><topic>β-Catenin</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Zhao, Guangze</creatorcontrib><creatorcontrib>Qiu, Ye</creatorcontrib><creatorcontrib>Zhang, Huifang M.</creatorcontrib><creatorcontrib>Yang, Decheng</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>ProQuest_Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>Research Library (Alumni Edition)</collection><collection>ProQuest Central (Alumni)</collection><collection>ProQuest Central</collection><collection>ProQuest Central Essentials</collection><collection>AUTh Library subscriptions: ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>Research Library Prep</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>PML(ProQuest Medical Library)</collection><collection>ProQuest_Research Library</collection><collection>Research Library (Corporate)</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>ProQuest Central Basic</collection><collection>MEDLINE - Academic</collection><jtitle>Heart failure reviews</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Zhao, Guangze</au><au>Qiu, Ye</au><au>Zhang, Huifang M.</au><au>Yang, Decheng</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Intercalated discs: cellular adhesion and signaling in heart health and diseases</atitle><jtitle>Heart failure reviews</jtitle><stitle>Heart Fail Rev</stitle><addtitle>Heart Fail Rev</addtitle><date>2019</date><risdate>2019</risdate><volume>24</volume><issue>1</issue><spage>115</spage><epage>132</epage><pages>115-132</pages><issn>1382-4147</issn><eissn>1573-7322</eissn><abstract>Intercalated discs (ICDs) are highly orchestrated structures that connect neighboring cardiomyocytes in the heart. Three major complexes are distinguished in ICD: desmosome, adherens junction (AJ), and gap junction (GJ). Desmosomes are major cell adhesion junctions that anchor cell membrane to the intermediate filament network; AJs connect the actin cytoskeleton of adjacent cells; and gap junctions metabolically and electrically connect the cytoplasm of adjacent cardiomyocytes. All these complexes work as a single unit, the so-called area composita, interdependently rather than individually. Mutation or altered expression of ICD proteins results in various cardiac diseases, such as ARVC (arrhythmogenic right ventricular cardiomyopathy), dilated cardiomyopathy, and hypotrophy cardiomyopathy, eventually leading to heart failure. In this article, we first review the recent findings on the structural organization of ICD and their functions and then focus on the recent advances in molecular pathogenesis of the ICD-related heart diseases, which include two major areas: i) the ICD gene mutations in cardiac diseases, and ii) the involvement of ICD proteins in signal transduction pathways leading to myocardium remodeling and eventual heart failure. These major ICD-related signaling pathways include Wnt/β-catenin pathway, p38 MAPK cascade, Rho-dependent serum response factor (SRF) signaling, calcineurin/NFAT signaling, Hippo kinase cascade, etc., which are differentially regulated in pathological conditions.</abstract><cop>New York</cop><pub>Springer US</pub><pmid>30288656</pmid><doi>10.1007/s10741-018-9743-7</doi><tpages>18</tpages><orcidid>https://orcid.org/0000-0002-3177-0070</orcidid></addata></record> |
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subjects | Actin Adherens Junctions - chemistry Adherens Junctions - genetics Adherens Junctions - metabolism Animals Calcineurin Cardiology Cardiomyocytes Cardiomyopathy Cell Adhesion Cell adhesion & migration Cell membranes Coronary artery disease Cytoplasm Cytoskeleton Desmosomes Desmosomes - chemistry Desmosomes - genetics Desmosomes - metabolism Dilated cardiomyopathy Gap junctions Gap Junctions - chemistry Gap Junctions - genetics Gap Junctions - metabolism Heart diseases Heart Diseases - genetics Heart Diseases - metabolism Heart failure Humans Kinases MAP kinase Medicine Medicine & Public Health Mutation Mutation, Missense Myocardium Myocardium - metabolism Myocytes, Cardiac - metabolism NF-AT protein Serum response factor Signal Transduction Ventricle Wnt protein β-Catenin |
title | Intercalated discs: cellular adhesion and signaling in heart health and diseases |
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