Loading…
The role of post‐translational modifications in cardiac hypertrophy
Pathological cardiac hypertrophy involves excessive protein synthesis, increased cardiac myocyte size and ultimately the development of heart failure. Thus, pathological cardiac hypertrophy is a major risk factor for many cardiovascular diseases and death in humans. Extensive research in the last de...
Saved in:
Published in: | Journal of cellular and molecular medicine 2019-06, Vol.23 (6), p.3795-3807 |
---|---|
Main Authors: | , , |
Format: | Article |
Language: | English |
Subjects: | |
Citations: | Items that this one cites Items that cite this one |
Online Access: | Get full text |
Tags: |
Add Tag
No Tags, Be the first to tag this record!
|
cited_by | cdi_FETCH-LOGICAL-c5550-ff3c59a417c356bfe9ed9b0229359f1588c13a4d20b2ce20b1895db3f1c833313 |
---|---|
cites | cdi_FETCH-LOGICAL-c5550-ff3c59a417c356bfe9ed9b0229359f1588c13a4d20b2ce20b1895db3f1c833313 |
container_end_page | 3807 |
container_issue | 6 |
container_start_page | 3795 |
container_title | Journal of cellular and molecular medicine |
container_volume | 23 |
creator | Yan, Kaowen Wang, Kun Li, Peifeng |
description | Pathological cardiac hypertrophy involves excessive protein synthesis, increased cardiac myocyte size and ultimately the development of heart failure. Thus, pathological cardiac hypertrophy is a major risk factor for many cardiovascular diseases and death in humans. Extensive research in the last decade has revealed that post‐translational modifications (PTMs), including phosphorylation, ubiquitination, SUMOylation, O‐GlcNAcylation, methylation and acetylation, play important roles in pathological cardiac hypertrophy pathways. These PTMs potently mediate myocardial hypertrophy responses via the interaction, stability, degradation, cellular translocation and activation of receptors, adaptors and signal transduction events. These changes occur in response to pathological hypertrophy stimuli. In this review, we summarize the roles of PTMs in regulating the development of pathological cardiac hypertrophy. Furthermore, PTMs are discussed as potential targets for treating or preventing cardiac hypertrophy. |
doi_str_mv | 10.1111/jcmm.14330 |
format | article |
fullrecord | <record><control><sourceid>proquest_pubme</sourceid><recordid>TN_cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_6533522</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>2204686850</sourcerecordid><originalsourceid>FETCH-LOGICAL-c5550-ff3c59a417c356bfe9ed9b0229359f1588c13a4d20b2ce20b1895db3f1c833313</originalsourceid><addsrcrecordid>eNp9kd1KBCEYhiWK_k-6gBjoJIIt9RsnPQli6ZeikzoWx9HWZWacdLbYsy6ha-xKctstqoM80E98eHjxRWiH4EOS1tFYN80hyQHwElonjNNBLiBfXsyEA19DGzGOMYaCgFhFa4AFw5SQdXR2PzJZ8LXJvM06H_v317c-qDbWqne-VXXW-MpZpz-vMXNtplWonNLZaNqZ0AffjaZbaMWqOprtxbmJHs7P7oeXg5u7i6vh6c1AM8bwwFrQTKicHGtgRWmNMJUoMaUCmLApLdcEVF5RXFJt0k64YFUJlmgOAAQ20cnc203KxlTatClrLbvgGhWm0isnf7-0biQf_bMsGACjNAn2F4LgnyYm9rJxUZu6Vq3xkygpxXnBC85wQvf-oGM_CelHZhQVDI45Fok6mFM6-BiDsd9hCJazduSsHfnZToJ3f8b_Rr_qSACZAy-uNtN_VPJ6eHs7l34AclGbig</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>2229537809</pqid></control><display><type>article</type><title>The role of post‐translational modifications in cardiac hypertrophy</title><source>Wiley-Blackwell Open Access Collection</source><source>Publicly Available Content Database (Proquest) (PQ_SDU_P3)</source><source>PubMed Central (Open access)</source><creator>Yan, Kaowen ; Wang, Kun ; Li, Peifeng</creator><creatorcontrib>Yan, Kaowen ; Wang, Kun ; Li, Peifeng</creatorcontrib><description>Pathological cardiac hypertrophy involves excessive protein synthesis, increased cardiac myocyte size and ultimately the development of heart failure. Thus, pathological cardiac hypertrophy is a major risk factor for many cardiovascular diseases and death in humans. Extensive research in the last decade has revealed that post‐translational modifications (PTMs), including phosphorylation, ubiquitination, SUMOylation, O‐GlcNAcylation, methylation and acetylation, play important roles in pathological cardiac hypertrophy pathways. These PTMs potently mediate myocardial hypertrophy responses via the interaction, stability, degradation, cellular translocation and activation of receptors, adaptors and signal transduction events. These changes occur in response to pathological hypertrophy stimuli. In this review, we summarize the roles of PTMs in regulating the development of pathological cardiac hypertrophy. Furthermore, PTMs are discussed as potential targets for treating or preventing cardiac hypertrophy.</description><identifier>ISSN: 1582-1838</identifier><identifier>EISSN: 1582-4934</identifier><identifier>DOI: 10.1111/jcmm.14330</identifier><identifier>PMID: 30950211</identifier><language>eng</language><publisher>England: John Wiley & Sons, Inc</publisher><subject>Acetylation ; Acetylglucosamine - metabolism ; Animals ; cardiac hypertrophy ; Cardiomegaly - genetics ; Cardiomegaly - metabolism ; Dual-Specificity Phosphatases - genetics ; Dual-Specificity Phosphatases - metabolism ; heart failure ; Histone Deacetylases - genetics ; Histone Deacetylases - metabolism ; Humans ; Methylation ; Myocytes, Cardiac - chemistry ; Myocytes, Cardiac - metabolism ; Phosphorylation ; post‐translational modifications (PTMs) ; Protein Processing, Post-Translational ; Review ; Reviews ; Signal Transduction ; Sumoylation ; Ubiquitin-Protein Ligases - genetics ; Ubiquitin-Protein Ligases - metabolism ; Ubiquitination</subject><ispartof>Journal of cellular and molecular medicine, 2019-06, Vol.23 (6), p.3795-3807</ispartof><rights>2019 The Authors. Journal of Cellular and Molecular Medicine published by John Wiley & Sons Ltd and Foundation for Cellular and Molecular Medicine.</rights><rights>2019. This work is published under http://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c5550-ff3c59a417c356bfe9ed9b0229359f1588c13a4d20b2ce20b1895db3f1c833313</citedby><cites>FETCH-LOGICAL-c5550-ff3c59a417c356bfe9ed9b0229359f1588c13a4d20b2ce20b1895db3f1c833313</cites><orcidid>0000-0002-4234-5571</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.proquest.com/docview/2229537809/fulltextPDF?pq-origsite=primo$$EPDF$$P50$$Gproquest$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.proquest.com/docview/2229537809?pq-origsite=primo$$EHTML$$P50$$Gproquest$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,881,11540,25730,27900,27901,36988,36989,44565,46026,46450,53765,53767,75095</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/30950211$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Yan, Kaowen</creatorcontrib><creatorcontrib>Wang, Kun</creatorcontrib><creatorcontrib>Li, Peifeng</creatorcontrib><title>The role of post‐translational modifications in cardiac hypertrophy</title><title>Journal of cellular and molecular medicine</title><addtitle>J Cell Mol Med</addtitle><description>Pathological cardiac hypertrophy involves excessive protein synthesis, increased cardiac myocyte size and ultimately the development of heart failure. Thus, pathological cardiac hypertrophy is a major risk factor for many cardiovascular diseases and death in humans. Extensive research in the last decade has revealed that post‐translational modifications (PTMs), including phosphorylation, ubiquitination, SUMOylation, O‐GlcNAcylation, methylation and acetylation, play important roles in pathological cardiac hypertrophy pathways. These PTMs potently mediate myocardial hypertrophy responses via the interaction, stability, degradation, cellular translocation and activation of receptors, adaptors and signal transduction events. These changes occur in response to pathological hypertrophy stimuli. In this review, we summarize the roles of PTMs in regulating the development of pathological cardiac hypertrophy. Furthermore, PTMs are discussed as potential targets for treating or preventing cardiac hypertrophy.</description><subject>Acetylation</subject><subject>Acetylglucosamine - metabolism</subject><subject>Animals</subject><subject>cardiac hypertrophy</subject><subject>Cardiomegaly - genetics</subject><subject>Cardiomegaly - metabolism</subject><subject>Dual-Specificity Phosphatases - genetics</subject><subject>Dual-Specificity Phosphatases - metabolism</subject><subject>heart failure</subject><subject>Histone Deacetylases - genetics</subject><subject>Histone Deacetylases - metabolism</subject><subject>Humans</subject><subject>Methylation</subject><subject>Myocytes, Cardiac - chemistry</subject><subject>Myocytes, Cardiac - metabolism</subject><subject>Phosphorylation</subject><subject>post‐translational modifications (PTMs)</subject><subject>Protein Processing, Post-Translational</subject><subject>Review</subject><subject>Reviews</subject><subject>Signal Transduction</subject><subject>Sumoylation</subject><subject>Ubiquitin-Protein Ligases - genetics</subject><subject>Ubiquitin-Protein Ligases - metabolism</subject><subject>Ubiquitination</subject><issn>1582-1838</issn><issn>1582-4934</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2019</creationdate><recordtype>article</recordtype><sourceid>24P</sourceid><sourceid>PIMPY</sourceid><recordid>eNp9kd1KBCEYhiWK_k-6gBjoJIIt9RsnPQli6ZeikzoWx9HWZWacdLbYsy6ha-xKctstqoM80E98eHjxRWiH4EOS1tFYN80hyQHwElonjNNBLiBfXsyEA19DGzGOMYaCgFhFa4AFw5SQdXR2PzJZ8LXJvM06H_v317c-qDbWqne-VXXW-MpZpz-vMXNtplWonNLZaNqZ0AffjaZbaMWqOprtxbmJHs7P7oeXg5u7i6vh6c1AM8bwwFrQTKicHGtgRWmNMJUoMaUCmLApLdcEVF5RXFJt0k64YFUJlmgOAAQ20cnc203KxlTatClrLbvgGhWm0isnf7-0biQf_bMsGACjNAn2F4LgnyYm9rJxUZu6Vq3xkygpxXnBC85wQvf-oGM_CelHZhQVDI45Fok6mFM6-BiDsd9hCJazduSsHfnZToJ3f8b_Rr_qSACZAy-uNtN_VPJ6eHs7l34AclGbig</recordid><startdate>201906</startdate><enddate>201906</enddate><creator>Yan, Kaowen</creator><creator>Wang, Kun</creator><creator>Li, Peifeng</creator><general>John Wiley & Sons, Inc</general><general>John Wiley and Sons Inc</general><scope>24P</scope><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>7TK</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>88I</scope><scope>8AO</scope><scope>8FD</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M2P</scope><scope>M7P</scope><scope>P64</scope><scope>PHGZM</scope><scope>PHGZT</scope><scope>PIMPY</scope><scope>PJZUB</scope><scope>PKEHL</scope><scope>PPXIY</scope><scope>PQEST</scope><scope>PQGLB</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>RC3</scope><scope>7X8</scope><scope>5PM</scope><orcidid>https://orcid.org/0000-0002-4234-5571</orcidid></search><sort><creationdate>201906</creationdate><title>The role of post‐translational modifications in cardiac hypertrophy</title><author>Yan, Kaowen ; Wang, Kun ; Li, Peifeng</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c5550-ff3c59a417c356bfe9ed9b0229359f1588c13a4d20b2ce20b1895db3f1c833313</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2019</creationdate><topic>Acetylation</topic><topic>Acetylglucosamine - metabolism</topic><topic>Animals</topic><topic>cardiac hypertrophy</topic><topic>Cardiomegaly - genetics</topic><topic>Cardiomegaly - metabolism</topic><topic>Dual-Specificity Phosphatases - genetics</topic><topic>Dual-Specificity Phosphatases - metabolism</topic><topic>heart failure</topic><topic>Histone Deacetylases - genetics</topic><topic>Histone Deacetylases - metabolism</topic><topic>Humans</topic><topic>Methylation</topic><topic>Myocytes, Cardiac - chemistry</topic><topic>Myocytes, Cardiac - metabolism</topic><topic>Phosphorylation</topic><topic>post‐translational modifications (PTMs)</topic><topic>Protein Processing, Post-Translational</topic><topic>Review</topic><topic>Reviews</topic><topic>Signal Transduction</topic><topic>Sumoylation</topic><topic>Ubiquitin-Protein Ligases - genetics</topic><topic>Ubiquitin-Protein Ligases - metabolism</topic><topic>Ubiquitination</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Yan, Kaowen</creatorcontrib><creatorcontrib>Wang, Kun</creatorcontrib><creatorcontrib>Li, Peifeng</creatorcontrib><collection>Wiley-Blackwell Open Access Collection</collection><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>Neurosciences Abstracts</collection><collection>Health Medical collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Science Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Technology Research Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>ProQuest Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central</collection><collection>Engineering Research Database</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>SciTech Premium Collection (Proquest) (PQ_SDU_P3)</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Biological Sciences</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>PML(ProQuest Medical Library)</collection><collection>ProQuest Science Journals</collection><collection>Biological Science Database</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>ProQuest Central (New)</collection><collection>ProQuest One Academic (New)</collection><collection>Publicly Available Content Database (Proquest) (PQ_SDU_P3)</collection><collection>ProQuest Health & Medical Research Collection</collection><collection>ProQuest One Academic Middle East (New)</collection><collection>ProQuest One Health & Nursing</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Applied & Life Sciences</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>ProQuest Central Basic</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Journal of cellular and molecular medicine</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Yan, Kaowen</au><au>Wang, Kun</au><au>Li, Peifeng</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>The role of post‐translational modifications in cardiac hypertrophy</atitle><jtitle>Journal of cellular and molecular medicine</jtitle><addtitle>J Cell Mol Med</addtitle><date>2019-06</date><risdate>2019</risdate><volume>23</volume><issue>6</issue><spage>3795</spage><epage>3807</epage><pages>3795-3807</pages><issn>1582-1838</issn><eissn>1582-4934</eissn><abstract>Pathological cardiac hypertrophy involves excessive protein synthesis, increased cardiac myocyte size and ultimately the development of heart failure. Thus, pathological cardiac hypertrophy is a major risk factor for many cardiovascular diseases and death in humans. Extensive research in the last decade has revealed that post‐translational modifications (PTMs), including phosphorylation, ubiquitination, SUMOylation, O‐GlcNAcylation, methylation and acetylation, play important roles in pathological cardiac hypertrophy pathways. These PTMs potently mediate myocardial hypertrophy responses via the interaction, stability, degradation, cellular translocation and activation of receptors, adaptors and signal transduction events. These changes occur in response to pathological hypertrophy stimuli. In this review, we summarize the roles of PTMs in regulating the development of pathological cardiac hypertrophy. Furthermore, PTMs are discussed as potential targets for treating or preventing cardiac hypertrophy.</abstract><cop>England</cop><pub>John Wiley & Sons, Inc</pub><pmid>30950211</pmid><doi>10.1111/jcmm.14330</doi><tpages>13</tpages><orcidid>https://orcid.org/0000-0002-4234-5571</orcidid><oa>free_for_read</oa></addata></record> |
fulltext | fulltext |
identifier | ISSN: 1582-1838 |
ispartof | Journal of cellular and molecular medicine, 2019-06, Vol.23 (6), p.3795-3807 |
issn | 1582-1838 1582-4934 |
language | eng |
recordid | cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_6533522 |
source | Wiley-Blackwell Open Access Collection; Publicly Available Content Database (Proquest) (PQ_SDU_P3); PubMed Central (Open access) |
subjects | Acetylation Acetylglucosamine - metabolism Animals cardiac hypertrophy Cardiomegaly - genetics Cardiomegaly - metabolism Dual-Specificity Phosphatases - genetics Dual-Specificity Phosphatases - metabolism heart failure Histone Deacetylases - genetics Histone Deacetylases - metabolism Humans Methylation Myocytes, Cardiac - chemistry Myocytes, Cardiac - metabolism Phosphorylation post‐translational modifications (PTMs) Protein Processing, Post-Translational Review Reviews Signal Transduction Sumoylation Ubiquitin-Protein Ligases - genetics Ubiquitin-Protein Ligases - metabolism Ubiquitination |
title | The role of post‐translational modifications in cardiac hypertrophy |
url | http://sfxeu10.hosted.exlibrisgroup.com/loughborough?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-02-24T21%3A05%3A35IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_pubme&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=The%20role%20of%20post%E2%80%90translational%20modifications%20in%20cardiac%20hypertrophy&rft.jtitle=Journal%20of%20cellular%20and%20molecular%20medicine&rft.au=Yan,%20Kaowen&rft.date=2019-06&rft.volume=23&rft.issue=6&rft.spage=3795&rft.epage=3807&rft.pages=3795-3807&rft.issn=1582-1838&rft.eissn=1582-4934&rft_id=info:doi/10.1111/jcmm.14330&rft_dat=%3Cproquest_pubme%3E2204686850%3C/proquest_pubme%3E%3Cgrp_id%3Ecdi_FETCH-LOGICAL-c5550-ff3c59a417c356bfe9ed9b0229359f1588c13a4d20b2ce20b1895db3f1c833313%3C/grp_id%3E%3Coa%3E%3C/oa%3E%3Curl%3E%3C/url%3E&rft_id=info:oai/&rft_pqid=2229537809&rft_id=info:pmid/30950211&rfr_iscdi=true |