CaMKII inhibition protects against hyperthyroid arrhythmias and adverse myocardial remodeling
Hyperthyroidism can potentiate arrhythmias and cardiac hypertrophy, whereas Ca2+/calmodulin-dependent kinase II (CaMKII) promotes maladaptive myocardial remodeling. However, it remains unclear whether CaMKII contributes to the progression of hyperthyroid heart disease (HHD). This study demonstrated...
Gespeichert in:
| Veröffentlicht in: | Biochemical and biophysical research communications 2022-07, Vol.615, p.136-142 |
|---|---|
| Hauptverfasser: | , , , , , , , , , , , , |
| Format: | Artikel |
| Sprache: | eng |
| Schlagworte: | |
| Online-Zugang: | Volltext |
| Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
| container_end_page | 142 |
|---|---|
| container_issue | |
| container_start_page | 136 |
| container_title | Biochemical and biophysical research communications |
| container_volume | 615 |
| creator | Nie, Daan Xia, Chaorui Wang, Zhiyu Ding, Peiwu Meng, Yidi Liu, Jie Li, Ting Gan, Ting Xuan, Baijun Huang, Yun Zhang, Jiaming Su, Guanhua Li, Jingdong |
| description | Hyperthyroidism can potentiate arrhythmias and cardiac hypertrophy, whereas Ca2+/calmodulin-dependent kinase II (CaMKII) promotes maladaptive myocardial remodeling. However, it remains unclear whether CaMKII contributes to the progression of hyperthyroid heart disease (HHD). This study demonstrated that CaMKII inhibition can relieve adverse myocardial remodeling and reduce sinus tachycardia, isoproterenol-induced atrial fibrillation, and ventricular arrhythmias in hyperthyroid mice with preserved heart function. Hyperthyroid cardiac hypertrophy was promoted by CaMKII upregulation-induced HDAC4/MEF2a activation. Briefly, CaMKII inhibition benefits HHD management greatly in mice by preventing arrhythmias and maladaptive remodeling.
•Hyperthyroid heart disease (HHD) was developed in mice by T4 administration.•HHD was characterized by tachyarrhythmias and adverse myocardial remodeling.•T4 promoted CaMKII expression to derepress HDAC4/MEF2a for HHD progression.•CaMKII inhibition ameliorated HHD greatly and is a promising treatment target. |
| doi_str_mv | 10.1016/j.bbrc.2022.04.082 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_2671268721</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><els_id>S0006291X22006179</els_id><sourcerecordid>2671268721</sourcerecordid><originalsourceid>FETCH-LOGICAL-c433t-9d64229feb6097758ff9206145c25a4cbdbb787d0145527de6c1f64ccb87a4183</originalsourceid><addsrcrecordid>eNqNkc1r3DAQxUVISTZp_oEcio-52B1pZcmGXsqStEsTekmhlyL0MV5r8cdW8gb830fLbnosOQ0z_N5jeI-QWwoFBSo-bwtjgi0YMFYAL6BiZ2RBoYacUeDnZAEAImc1_X1JrmLcAlDKRX1BLpeloLICWJA_K_30Y73O_NB64yc_DtkujBPaKWZ6o_0Qp6yddximdg6jd5kOoZ2ntvc6AUPa3QuGiFk_j1YH53WXBexHh50fNh_Jh0Z3EW9O85r8erh_Xn3PH39-W6--PuaWL5dTXjvBGasbNAJqKcuqaWoGgvLSslJza5wxspIO0qVk0qGwtBHcWlNJzWm1vCZ3R9_0-989xkn1PlrsOj3guI-KCUmZqCSj70DTD1UteZlQdkRtGGMM2Khd8L0Os6KgDg2orTo0oA4NKOAqNZBEn07-e9Oj-yd5izwBX44ApkBePAYVrcfBovMhxa7c6P_n_wrmKZfF</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>2660989745</pqid></control><display><type>article</type><title>CaMKII inhibition protects against hyperthyroid arrhythmias and adverse myocardial remodeling</title><source>Elsevier ScienceDirect Journals</source><creator>Nie, Daan ; Xia, Chaorui ; Wang, Zhiyu ; Ding, Peiwu ; Meng, Yidi ; Liu, Jie ; Li, Ting ; Gan, Ting ; Xuan, Baijun ; Huang, Yun ; Zhang, Jiaming ; Su, Guanhua ; Li, Jingdong</creator><creatorcontrib>Nie, Daan ; Xia, Chaorui ; Wang, Zhiyu ; Ding, Peiwu ; Meng, Yidi ; Liu, Jie ; Li, Ting ; Gan, Ting ; Xuan, Baijun ; Huang, Yun ; Zhang, Jiaming ; Su, Guanhua ; Li, Jingdong</creatorcontrib><description>Hyperthyroidism can potentiate arrhythmias and cardiac hypertrophy, whereas Ca2+/calmodulin-dependent kinase II (CaMKII) promotes maladaptive myocardial remodeling. However, it remains unclear whether CaMKII contributes to the progression of hyperthyroid heart disease (HHD). This study demonstrated that CaMKII inhibition can relieve adverse myocardial remodeling and reduce sinus tachycardia, isoproterenol-induced atrial fibrillation, and ventricular arrhythmias in hyperthyroid mice with preserved heart function. Hyperthyroid cardiac hypertrophy was promoted by CaMKII upregulation-induced HDAC4/MEF2a activation. Briefly, CaMKII inhibition benefits HHD management greatly in mice by preventing arrhythmias and maladaptive remodeling.
•Hyperthyroid heart disease (HHD) was developed in mice by T4 administration.•HHD was characterized by tachyarrhythmias and adverse myocardial remodeling.•T4 promoted CaMKII expression to derepress HDAC4/MEF2a for HHD progression.•CaMKII inhibition ameliorated HHD greatly and is a promising treatment target.</description><identifier>ISSN: 0006-291X</identifier><identifier>EISSN: 1090-2104</identifier><identifier>DOI: 10.1016/j.bbrc.2022.04.082</identifier><identifier>PMID: 35617800</identifier><language>eng</language><publisher>United States: Elsevier Inc</publisher><subject>Adverse myocardial remodeling ; atrial fibrillation ; calcium-calmodulin-dependent protein kinase ; CaMKII ; HDAC4 ; heart ; Hyperthyroid heart disease (HHD) ; hyperthyroidism ; hypertrophy ; MEF2a ; Sinus tachycardia ; tachycardia</subject><ispartof>Biochemical and biophysical research communications, 2022-07, Vol.615, p.136-142</ispartof><rights>2022 The Authors</rights><rights>Copyright © 2022 The Authors. Published by Elsevier Inc. All rights reserved.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c433t-9d64229feb6097758ff9206145c25a4cbdbb787d0145527de6c1f64ccb87a4183</citedby><cites>FETCH-LOGICAL-c433t-9d64229feb6097758ff9206145c25a4cbdbb787d0145527de6c1f64ccb87a4183</cites><orcidid>0000-0003-3914-5074 ; 0000-0001-8793-8146</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/S0006291X22006179$$EHTML$$P50$$Gelsevier$$Hfree_for_read</linktohtml><link.rule.ids>314,776,780,3537,27903,27904,65309</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/35617800$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Nie, Daan</creatorcontrib><creatorcontrib>Xia, Chaorui</creatorcontrib><creatorcontrib>Wang, Zhiyu</creatorcontrib><creatorcontrib>Ding, Peiwu</creatorcontrib><creatorcontrib>Meng, Yidi</creatorcontrib><creatorcontrib>Liu, Jie</creatorcontrib><creatorcontrib>Li, Ting</creatorcontrib><creatorcontrib>Gan, Ting</creatorcontrib><creatorcontrib>Xuan, Baijun</creatorcontrib><creatorcontrib>Huang, Yun</creatorcontrib><creatorcontrib>Zhang, Jiaming</creatorcontrib><creatorcontrib>Su, Guanhua</creatorcontrib><creatorcontrib>Li, Jingdong</creatorcontrib><title>CaMKII inhibition protects against hyperthyroid arrhythmias and adverse myocardial remodeling</title><title>Biochemical and biophysical research communications</title><addtitle>Biochem Biophys Res Commun</addtitle><description>Hyperthyroidism can potentiate arrhythmias and cardiac hypertrophy, whereas Ca2+/calmodulin-dependent kinase II (CaMKII) promotes maladaptive myocardial remodeling. However, it remains unclear whether CaMKII contributes to the progression of hyperthyroid heart disease (HHD). This study demonstrated that CaMKII inhibition can relieve adverse myocardial remodeling and reduce sinus tachycardia, isoproterenol-induced atrial fibrillation, and ventricular arrhythmias in hyperthyroid mice with preserved heart function. Hyperthyroid cardiac hypertrophy was promoted by CaMKII upregulation-induced HDAC4/MEF2a activation. Briefly, CaMKII inhibition benefits HHD management greatly in mice by preventing arrhythmias and maladaptive remodeling.
•Hyperthyroid heart disease (HHD) was developed in mice by T4 administration.•HHD was characterized by tachyarrhythmias and adverse myocardial remodeling.•T4 promoted CaMKII expression to derepress HDAC4/MEF2a for HHD progression.•CaMKII inhibition ameliorated HHD greatly and is a promising treatment target.</description><subject>Adverse myocardial remodeling</subject><subject>atrial fibrillation</subject><subject>calcium-calmodulin-dependent protein kinase</subject><subject>CaMKII</subject><subject>HDAC4</subject><subject>heart</subject><subject>Hyperthyroid heart disease (HHD)</subject><subject>hyperthyroidism</subject><subject>hypertrophy</subject><subject>MEF2a</subject><subject>Sinus tachycardia</subject><subject>tachycardia</subject><issn>0006-291X</issn><issn>1090-2104</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2022</creationdate><recordtype>article</recordtype><recordid>eNqNkc1r3DAQxUVISTZp_oEcio-52B1pZcmGXsqStEsTekmhlyL0MV5r8cdW8gb830fLbnosOQ0z_N5jeI-QWwoFBSo-bwtjgi0YMFYAL6BiZ2RBoYacUeDnZAEAImc1_X1JrmLcAlDKRX1BLpeloLICWJA_K_30Y73O_NB64yc_DtkujBPaKWZ6o_0Qp6yddximdg6jd5kOoZ2ntvc6AUPa3QuGiFk_j1YH53WXBexHh50fNh_Jh0Z3EW9O85r8erh_Xn3PH39-W6--PuaWL5dTXjvBGasbNAJqKcuqaWoGgvLSslJza5wxspIO0qVk0qGwtBHcWlNJzWm1vCZ3R9_0-989xkn1PlrsOj3guI-KCUmZqCSj70DTD1UteZlQdkRtGGMM2Khd8L0Os6KgDg2orTo0oA4NKOAqNZBEn07-e9Oj-yd5izwBX44ApkBePAYVrcfBovMhxa7c6P_n_wrmKZfF</recordid><startdate>20220730</startdate><enddate>20220730</enddate><creator>Nie, Daan</creator><creator>Xia, Chaorui</creator><creator>Wang, Zhiyu</creator><creator>Ding, Peiwu</creator><creator>Meng, Yidi</creator><creator>Liu, Jie</creator><creator>Li, Ting</creator><creator>Gan, Ting</creator><creator>Xuan, Baijun</creator><creator>Huang, Yun</creator><creator>Zhang, Jiaming</creator><creator>Su, Guanhua</creator><creator>Li, Jingdong</creator><general>Elsevier Inc</general><scope>6I.</scope><scope>AAFTH</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7S9</scope><scope>L.6</scope><scope>7X8</scope><orcidid>https://orcid.org/0000-0003-3914-5074</orcidid><orcidid>https://orcid.org/0000-0001-8793-8146</orcidid></search><sort><creationdate>20220730</creationdate><title>CaMKII inhibition protects against hyperthyroid arrhythmias and adverse myocardial remodeling</title><author>Nie, Daan ; Xia, Chaorui ; Wang, Zhiyu ; Ding, Peiwu ; Meng, Yidi ; Liu, Jie ; Li, Ting ; Gan, Ting ; Xuan, Baijun ; Huang, Yun ; Zhang, Jiaming ; Su, Guanhua ; Li, Jingdong</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c433t-9d64229feb6097758ff9206145c25a4cbdbb787d0145527de6c1f64ccb87a4183</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2022</creationdate><topic>Adverse myocardial remodeling</topic><topic>atrial fibrillation</topic><topic>calcium-calmodulin-dependent protein kinase</topic><topic>CaMKII</topic><topic>HDAC4</topic><topic>heart</topic><topic>Hyperthyroid heart disease (HHD)</topic><topic>hyperthyroidism</topic><topic>hypertrophy</topic><topic>MEF2a</topic><topic>Sinus tachycardia</topic><topic>tachycardia</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Nie, Daan</creatorcontrib><creatorcontrib>Xia, Chaorui</creatorcontrib><creatorcontrib>Wang, Zhiyu</creatorcontrib><creatorcontrib>Ding, Peiwu</creatorcontrib><creatorcontrib>Meng, Yidi</creatorcontrib><creatorcontrib>Liu, Jie</creatorcontrib><creatorcontrib>Li, Ting</creatorcontrib><creatorcontrib>Gan, Ting</creatorcontrib><creatorcontrib>Xuan, Baijun</creatorcontrib><creatorcontrib>Huang, Yun</creatorcontrib><creatorcontrib>Zhang, Jiaming</creatorcontrib><creatorcontrib>Su, Guanhua</creatorcontrib><creatorcontrib>Li, Jingdong</creatorcontrib><collection>ScienceDirect Open Access Titles</collection><collection>Elsevier:ScienceDirect:Open Access</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>AGRICOLA</collection><collection>AGRICOLA - Academic</collection><collection>MEDLINE - Academic</collection><jtitle>Biochemical and biophysical research communications</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Nie, Daan</au><au>Xia, Chaorui</au><au>Wang, Zhiyu</au><au>Ding, Peiwu</au><au>Meng, Yidi</au><au>Liu, Jie</au><au>Li, Ting</au><au>Gan, Ting</au><au>Xuan, Baijun</au><au>Huang, Yun</au><au>Zhang, Jiaming</au><au>Su, Guanhua</au><au>Li, Jingdong</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>CaMKII inhibition protects against hyperthyroid arrhythmias and adverse myocardial remodeling</atitle><jtitle>Biochemical and biophysical research communications</jtitle><addtitle>Biochem Biophys Res Commun</addtitle><date>2022-07-30</date><risdate>2022</risdate><volume>615</volume><spage>136</spage><epage>142</epage><pages>136-142</pages><issn>0006-291X</issn><eissn>1090-2104</eissn><abstract>Hyperthyroidism can potentiate arrhythmias and cardiac hypertrophy, whereas Ca2+/calmodulin-dependent kinase II (CaMKII) promotes maladaptive myocardial remodeling. However, it remains unclear whether CaMKII contributes to the progression of hyperthyroid heart disease (HHD). This study demonstrated that CaMKII inhibition can relieve adverse myocardial remodeling and reduce sinus tachycardia, isoproterenol-induced atrial fibrillation, and ventricular arrhythmias in hyperthyroid mice with preserved heart function. Hyperthyroid cardiac hypertrophy was promoted by CaMKII upregulation-induced HDAC4/MEF2a activation. Briefly, CaMKII inhibition benefits HHD management greatly in mice by preventing arrhythmias and maladaptive remodeling.
•Hyperthyroid heart disease (HHD) was developed in mice by T4 administration.•HHD was characterized by tachyarrhythmias and adverse myocardial remodeling.•T4 promoted CaMKII expression to derepress HDAC4/MEF2a for HHD progression.•CaMKII inhibition ameliorated HHD greatly and is a promising treatment target.</abstract><cop>United States</cop><pub>Elsevier Inc</pub><pmid>35617800</pmid><doi>10.1016/j.bbrc.2022.04.082</doi><tpages>7</tpages><orcidid>https://orcid.org/0000-0003-3914-5074</orcidid><orcidid>https://orcid.org/0000-0001-8793-8146</orcidid><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 0006-291X |
| ispartof | Biochemical and biophysical research communications, 2022-07, Vol.615, p.136-142 |
| issn | 0006-291X 1090-2104 |
| language | eng |
| recordid | cdi_proquest_miscellaneous_2671268721 |
| source | Elsevier ScienceDirect Journals |
| subjects | Adverse myocardial remodeling atrial fibrillation calcium-calmodulin-dependent protein kinase CaMKII HDAC4 heart Hyperthyroid heart disease (HHD) hyperthyroidism hypertrophy MEF2a Sinus tachycardia tachycardia |
| title | CaMKII inhibition protects against hyperthyroid arrhythmias and adverse myocardial remodeling |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-28T07%3A20%3A45IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_cross&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=CaMKII%20inhibition%20protects%20against%20hyperthyroid%20arrhythmias%20and%20adverse%20myocardial%20remodeling&rft.jtitle=Biochemical%20and%20biophysical%20research%20communications&rft.au=Nie,%20Daan&rft.date=2022-07-30&rft.volume=615&rft.spage=136&rft.epage=142&rft.pages=136-142&rft.issn=0006-291X&rft.eissn=1090-2104&rft_id=info:doi/10.1016/j.bbrc.2022.04.082&rft_dat=%3Cproquest_cross%3E2671268721%3C/proquest_cross%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=2660989745&rft_id=info:pmid/35617800&rft_els_id=S0006291X22006179&rfr_iscdi=true |