Isoproterenol instigates cardiomyocyte apoptosis and heart failure via AMPK inactivation-mediated endoplasmic reticulum stress
A prolonged or excessive adrenergic activation leads to myocyte loss and heart dysfunction; however, how it contributes to heart failure remains poorly defined. Here we show that isoproterenol (ISO) induced aberrant endoplasmic reticulum (ER) stress and apoptotic cell death, which was inhibited by a...
Gespeichert in:
| Veröffentlicht in: | Apoptosis (London) 2013-07, Vol.18 (7), p.800-810 |
|---|---|
| Hauptverfasser: | , , , , , , , , , , |
| Format: | Artikel |
| Sprache: | eng |
| Schlagworte: | |
| Online-Zugang: | Volltext |
| Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
| container_end_page | 810 |
|---|---|
| container_issue | 7 |
| container_start_page | 800 |
| container_title | Apoptosis (London) |
| container_volume | 18 |
| creator | Zhuo, Xiao-Zhen Wu, Yue Ni, Ya-Juan Liu, Jun-Hui Gong, Min Wang, Xue-Hui Wei, Feng Wang, Ting-Zhong Yuan, Zuyi Ma, Ai-Qun Song, Ping |
| description | A prolonged or excessive adrenergic activation leads to myocyte loss and heart dysfunction; however, how it contributes to heart failure remains poorly defined. Here we show that isoproterenol (ISO) induced aberrant endoplasmic reticulum (ER) stress and apoptotic cell death, which was inhibited by activating the AMP-activated protein kinase (AMPK) in vitro and in vivo. Persistent ISO stimulation suppressed the AMPK phosphorylation and function, resulting in enhanced ER stress and the subsequent cell apoptosis in cardiomyocytes in vitro and in vivo. AMPK activation decreased the aberrant ER stress, apoptosis, and brain natriuretic peptide (BNP) release in ISO-treated cardiomyocytes, which was blocked by AMPK inhibitor Compound C. Importantly, increased ER stress and apoptosis were observed in ISO-treated cardiomyocytes isolated from AMPKα2
−/−
mice. Inhibition of ER stress attenuated the apoptosis but failed to reverse AMPK inhibition in ISO-treated cardiomyocytes. Moreover, metformin administration activated AMPK and reduced both ER stress and apoptosis in ISO-induced rat heart failure in vivo. We conclude that ISO, via AMPK inactivation, causes aberrant ER stress, cardiomyocyte injury, BNP release, apoptosis, and hence heart failure in vivo, all of which are inhibited by AMPK activation. |
| doi_str_mv | 10.1007/s10495-013-0843-5 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_journals_1356427130</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>2983014721</sourcerecordid><originalsourceid>FETCH-LOGICAL-c438t-7a9ade1a0bbb7119f5d0018c044ea5442086fc2e37d905f74d2d95ce438129d43</originalsourceid><addsrcrecordid>eNp1kE9rFTEUxYMotlY_gBsJuI7eTJL5syzFarFiFy24C3nJnZoyMxlzM4W38bM35VVx4-peuOecy_kx9lbCBwnQfSQJejACpBLQayXMM3YsTadE25kfz-uuWhC97M0Re0V0BwCqV_olO2pU24BW5pj9vqC05lQw45ImHhcq8dYVJO5dDjHN--T3Bblb01oSReJuCfwnulz46OK0ZeT30fHTb1dfq9v5Eu9diWkRM4ZYgwLHJaR1cjRHzzOW6LdpmzmVjESv2YvRTYRvnuYJuzn_dH32RVx-_3xxdnopvFZ9EZ0bXEDpYLfbdVIOowkAsvegNTqjdQN9O_oGVRcGMGOnQxMG47GaZTMErU7Y-0Nu7fprQyr2Lm15qS-tVKbVTScVVJU8qHxORBlHu-Y4u7y3EuwjcXsgbitx-0jcmup595S87Wrlv44_iKugOQionpZbzP-8_m_qA5cujoU</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>1356427130</pqid></control><display><type>article</type><title>Isoproterenol instigates cardiomyocyte apoptosis and heart failure via AMPK inactivation-mediated endoplasmic reticulum stress</title><source>MEDLINE</source><source>SpringerLink Journals</source><creator>Zhuo, Xiao-Zhen ; Wu, Yue ; Ni, Ya-Juan ; Liu, Jun-Hui ; Gong, Min ; Wang, Xue-Hui ; Wei, Feng ; Wang, Ting-Zhong ; Yuan, Zuyi ; Ma, Ai-Qun ; Song, Ping</creator><creatorcontrib>Zhuo, Xiao-Zhen ; Wu, Yue ; Ni, Ya-Juan ; Liu, Jun-Hui ; Gong, Min ; Wang, Xue-Hui ; Wei, Feng ; Wang, Ting-Zhong ; Yuan, Zuyi ; Ma, Ai-Qun ; Song, Ping</creatorcontrib><description>A prolonged or excessive adrenergic activation leads to myocyte loss and heart dysfunction; however, how it contributes to heart failure remains poorly defined. Here we show that isoproterenol (ISO) induced aberrant endoplasmic reticulum (ER) stress and apoptotic cell death, which was inhibited by activating the AMP-activated protein kinase (AMPK) in vitro and in vivo. Persistent ISO stimulation suppressed the AMPK phosphorylation and function, resulting in enhanced ER stress and the subsequent cell apoptosis in cardiomyocytes in vitro and in vivo. AMPK activation decreased the aberrant ER stress, apoptosis, and brain natriuretic peptide (BNP) release in ISO-treated cardiomyocytes, which was blocked by AMPK inhibitor Compound C. Importantly, increased ER stress and apoptosis were observed in ISO-treated cardiomyocytes isolated from AMPKα2
−/−
mice. Inhibition of ER stress attenuated the apoptosis but failed to reverse AMPK inhibition in ISO-treated cardiomyocytes. Moreover, metformin administration activated AMPK and reduced both ER stress and apoptosis in ISO-induced rat heart failure in vivo. We conclude that ISO, via AMPK inactivation, causes aberrant ER stress, cardiomyocyte injury, BNP release, apoptosis, and hence heart failure in vivo, all of which are inhibited by AMPK activation.</description><identifier>ISSN: 1360-8185</identifier><identifier>EISSN: 1573-675X</identifier><identifier>DOI: 10.1007/s10495-013-0843-5</identifier><identifier>PMID: 23620435</identifier><language>eng</language><publisher>Boston: Springer US</publisher><subject>AMP-Activated Protein Kinases - antagonists & inhibitors ; AMP-Activated Protein Kinases - deficiency ; AMP-Activated Protein Kinases - genetics ; Animals ; Apoptosis - drug effects ; Biochemistry ; Biomedical and Life Sciences ; Biomedicine ; Cancer Research ; Cell Biology ; Endoplasmic Reticulum - drug effects ; Endoplasmic Reticulum - genetics ; Endoplasmic Reticulum - metabolism ; Endoplasmic Reticulum Stress - drug effects ; Gene Expression Regulation ; Heart Failure - chemically induced ; Heart Failure - enzymology ; Heart Failure - pathology ; Heart Failure - prevention & control ; Inactivation ; Isoproterenol - adverse effects ; Male ; Metformin - pharmacology ; Mice ; Mice, Knockout ; Myocardium - enzymology ; Myocardium - pathology ; Myocytes, Cardiac - drug effects ; Myocytes, Cardiac - enzymology ; Myocytes, Cardiac - pathology ; Natriuretic Peptide, Brain - metabolism ; Oncology ; Original Paper ; Phosphorylation ; Pyrazoles - pharmacology ; Pyrimidines - pharmacology ; Rats ; Rats, Sprague-Dawley ; Signal Transduction ; Stress ; Virology</subject><ispartof>Apoptosis (London), 2013-07, Vol.18 (7), p.800-810</ispartof><rights>Springer Science+Business Media New York 2013</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c438t-7a9ade1a0bbb7119f5d0018c044ea5442086fc2e37d905f74d2d95ce438129d43</citedby><cites>FETCH-LOGICAL-c438t-7a9ade1a0bbb7119f5d0018c044ea5442086fc2e37d905f74d2d95ce438129d43</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s10495-013-0843-5$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s10495-013-0843-5$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,777,781,27905,27906,41469,42538,51300</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/23620435$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Zhuo, Xiao-Zhen</creatorcontrib><creatorcontrib>Wu, Yue</creatorcontrib><creatorcontrib>Ni, Ya-Juan</creatorcontrib><creatorcontrib>Liu, Jun-Hui</creatorcontrib><creatorcontrib>Gong, Min</creatorcontrib><creatorcontrib>Wang, Xue-Hui</creatorcontrib><creatorcontrib>Wei, Feng</creatorcontrib><creatorcontrib>Wang, Ting-Zhong</creatorcontrib><creatorcontrib>Yuan, Zuyi</creatorcontrib><creatorcontrib>Ma, Ai-Qun</creatorcontrib><creatorcontrib>Song, Ping</creatorcontrib><title>Isoproterenol instigates cardiomyocyte apoptosis and heart failure via AMPK inactivation-mediated endoplasmic reticulum stress</title><title>Apoptosis (London)</title><addtitle>Apoptosis</addtitle><addtitle>Apoptosis</addtitle><description>A prolonged or excessive adrenergic activation leads to myocyte loss and heart dysfunction; however, how it contributes to heart failure remains poorly defined. Here we show that isoproterenol (ISO) induced aberrant endoplasmic reticulum (ER) stress and apoptotic cell death, which was inhibited by activating the AMP-activated protein kinase (AMPK) in vitro and in vivo. Persistent ISO stimulation suppressed the AMPK phosphorylation and function, resulting in enhanced ER stress and the subsequent cell apoptosis in cardiomyocytes in vitro and in vivo. AMPK activation decreased the aberrant ER stress, apoptosis, and brain natriuretic peptide (BNP) release in ISO-treated cardiomyocytes, which was blocked by AMPK inhibitor Compound C. Importantly, increased ER stress and apoptosis were observed in ISO-treated cardiomyocytes isolated from AMPKα2
−/−
mice. Inhibition of ER stress attenuated the apoptosis but failed to reverse AMPK inhibition in ISO-treated cardiomyocytes. Moreover, metformin administration activated AMPK and reduced both ER stress and apoptosis in ISO-induced rat heart failure in vivo. We conclude that ISO, via AMPK inactivation, causes aberrant ER stress, cardiomyocyte injury, BNP release, apoptosis, and hence heart failure in vivo, all of which are inhibited by AMPK activation.</description><subject>AMP-Activated Protein Kinases - antagonists & inhibitors</subject><subject>AMP-Activated Protein Kinases - deficiency</subject><subject>AMP-Activated Protein Kinases - genetics</subject><subject>Animals</subject><subject>Apoptosis - drug effects</subject><subject>Biochemistry</subject><subject>Biomedical and Life Sciences</subject><subject>Biomedicine</subject><subject>Cancer Research</subject><subject>Cell Biology</subject><subject>Endoplasmic Reticulum - drug effects</subject><subject>Endoplasmic Reticulum - genetics</subject><subject>Endoplasmic Reticulum - metabolism</subject><subject>Endoplasmic Reticulum Stress - drug effects</subject><subject>Gene Expression Regulation</subject><subject>Heart Failure - chemically induced</subject><subject>Heart Failure - enzymology</subject><subject>Heart Failure - pathology</subject><subject>Heart Failure - prevention & control</subject><subject>Inactivation</subject><subject>Isoproterenol - adverse effects</subject><subject>Male</subject><subject>Metformin - pharmacology</subject><subject>Mice</subject><subject>Mice, Knockout</subject><subject>Myocardium - enzymology</subject><subject>Myocardium - pathology</subject><subject>Myocytes, Cardiac - drug effects</subject><subject>Myocytes, Cardiac - enzymology</subject><subject>Myocytes, Cardiac - pathology</subject><subject>Natriuretic Peptide, Brain - metabolism</subject><subject>Oncology</subject><subject>Original Paper</subject><subject>Phosphorylation</subject><subject>Pyrazoles - pharmacology</subject><subject>Pyrimidines - pharmacology</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><subject>Signal Transduction</subject><subject>Stress</subject><subject>Virology</subject><issn>1360-8185</issn><issn>1573-675X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2013</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNp1kE9rFTEUxYMotlY_gBsJuI7eTJL5syzFarFiFy24C3nJnZoyMxlzM4W38bM35VVx4-peuOecy_kx9lbCBwnQfSQJejACpBLQayXMM3YsTadE25kfz-uuWhC97M0Re0V0BwCqV_olO2pU24BW5pj9vqC05lQw45ImHhcq8dYVJO5dDjHN--T3Bblb01oSReJuCfwnulz46OK0ZeT30fHTb1dfq9v5Eu9diWkRM4ZYgwLHJaR1cjRHzzOW6LdpmzmVjESv2YvRTYRvnuYJuzn_dH32RVx-_3xxdnopvFZ9EZ0bXEDpYLfbdVIOowkAsvegNTqjdQN9O_oGVRcGMGOnQxMG47GaZTMErU7Y-0Nu7fprQyr2Lm15qS-tVKbVTScVVJU8qHxORBlHu-Y4u7y3EuwjcXsgbitx-0jcmup595S87Wrlv44_iKugOQionpZbzP-8_m_qA5cujoU</recordid><startdate>20130701</startdate><enddate>20130701</enddate><creator>Zhuo, Xiao-Zhen</creator><creator>Wu, Yue</creator><creator>Ni, Ya-Juan</creator><creator>Liu, Jun-Hui</creator><creator>Gong, Min</creator><creator>Wang, Xue-Hui</creator><creator>Wei, Feng</creator><creator>Wang, Ting-Zhong</creator><creator>Yuan, Zuyi</creator><creator>Ma, Ai-Qun</creator><creator>Song, Ping</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>7QL</scope><scope>7QP</scope><scope>7RQ</scope><scope>7TK</scope><scope>7TM</scope><scope>7U9</scope><scope>7X7</scope><scope>7XB</scope><scope>88A</scope><scope>88E</scope><scope>8AO</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AEUYN</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>C1K</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M7N</scope><scope>M7P</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>Q9U</scope><scope>U9A</scope></search><sort><creationdate>20130701</creationdate><title>Isoproterenol instigates cardiomyocyte apoptosis and heart failure via AMPK inactivation-mediated endoplasmic reticulum stress</title><author>Zhuo, Xiao-Zhen ; Wu, Yue ; Ni, Ya-Juan ; Liu, Jun-Hui ; Gong, Min ; Wang, Xue-Hui ; Wei, Feng ; Wang, Ting-Zhong ; Yuan, Zuyi ; Ma, Ai-Qun ; Song, Ping</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c438t-7a9ade1a0bbb7119f5d0018c044ea5442086fc2e37d905f74d2d95ce438129d43</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2013</creationdate><topic>AMP-Activated Protein Kinases - antagonists & inhibitors</topic><topic>AMP-Activated Protein Kinases - deficiency</topic><topic>AMP-Activated Protein Kinases - genetics</topic><topic>Animals</topic><topic>Apoptosis - drug effects</topic><topic>Biochemistry</topic><topic>Biomedical and Life Sciences</topic><topic>Biomedicine</topic><topic>Cancer Research</topic><topic>Cell Biology</topic><topic>Endoplasmic Reticulum - drug effects</topic><topic>Endoplasmic Reticulum - genetics</topic><topic>Endoplasmic Reticulum - metabolism</topic><topic>Endoplasmic Reticulum Stress - drug effects</topic><topic>Gene Expression Regulation</topic><topic>Heart Failure - chemically induced</topic><topic>Heart Failure - enzymology</topic><topic>Heart Failure - pathology</topic><topic>Heart Failure - prevention & control</topic><topic>Inactivation</topic><topic>Isoproterenol - adverse effects</topic><topic>Male</topic><topic>Metformin - pharmacology</topic><topic>Mice</topic><topic>Mice, Knockout</topic><topic>Myocardium - enzymology</topic><topic>Myocardium - pathology</topic><topic>Myocytes, Cardiac - drug effects</topic><topic>Myocytes, Cardiac - enzymology</topic><topic>Myocytes, Cardiac - pathology</topic><topic>Natriuretic Peptide, Brain - metabolism</topic><topic>Oncology</topic><topic>Original Paper</topic><topic>Phosphorylation</topic><topic>Pyrazoles - pharmacology</topic><topic>Pyrimidines - pharmacology</topic><topic>Rats</topic><topic>Rats, Sprague-Dawley</topic><topic>Signal Transduction</topic><topic>Stress</topic><topic>Virology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Zhuo, Xiao-Zhen</creatorcontrib><creatorcontrib>Wu, Yue</creatorcontrib><creatorcontrib>Ni, Ya-Juan</creatorcontrib><creatorcontrib>Liu, Jun-Hui</creatorcontrib><creatorcontrib>Gong, Min</creatorcontrib><creatorcontrib>Wang, Xue-Hui</creatorcontrib><creatorcontrib>Wei, Feng</creatorcontrib><creatorcontrib>Wang, Ting-Zhong</creatorcontrib><creatorcontrib>Yuan, Zuyi</creatorcontrib><creatorcontrib>Ma, Ai-Qun</creatorcontrib><creatorcontrib>Song, Ping</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>Bacteriology Abstracts (Microbiology B)</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Career & Technical Education Database</collection><collection>Neurosciences Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Biology Database (Alumni Edition)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</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 Edition)</collection><collection>ProQuest One Sustainability</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>Environmental Sciences and Pollution Management</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Algology Mycology and Protozoology Abstracts (Microbiology C)</collection><collection>Biological Science Database</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 Basic</collection><jtitle>Apoptosis (London)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Zhuo, Xiao-Zhen</au><au>Wu, Yue</au><au>Ni, Ya-Juan</au><au>Liu, Jun-Hui</au><au>Gong, Min</au><au>Wang, Xue-Hui</au><au>Wei, Feng</au><au>Wang, Ting-Zhong</au><au>Yuan, Zuyi</au><au>Ma, Ai-Qun</au><au>Song, Ping</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Isoproterenol instigates cardiomyocyte apoptosis and heart failure via AMPK inactivation-mediated endoplasmic reticulum stress</atitle><jtitle>Apoptosis (London)</jtitle><stitle>Apoptosis</stitle><addtitle>Apoptosis</addtitle><date>2013-07-01</date><risdate>2013</risdate><volume>18</volume><issue>7</issue><spage>800</spage><epage>810</epage><pages>800-810</pages><issn>1360-8185</issn><eissn>1573-675X</eissn><abstract>A prolonged or excessive adrenergic activation leads to myocyte loss and heart dysfunction; however, how it contributes to heart failure remains poorly defined. Here we show that isoproterenol (ISO) induced aberrant endoplasmic reticulum (ER) stress and apoptotic cell death, which was inhibited by activating the AMP-activated protein kinase (AMPK) in vitro and in vivo. Persistent ISO stimulation suppressed the AMPK phosphorylation and function, resulting in enhanced ER stress and the subsequent cell apoptosis in cardiomyocytes in vitro and in vivo. AMPK activation decreased the aberrant ER stress, apoptosis, and brain natriuretic peptide (BNP) release in ISO-treated cardiomyocytes, which was blocked by AMPK inhibitor Compound C. Importantly, increased ER stress and apoptosis were observed in ISO-treated cardiomyocytes isolated from AMPKα2
−/−
mice. Inhibition of ER stress attenuated the apoptosis but failed to reverse AMPK inhibition in ISO-treated cardiomyocytes. Moreover, metformin administration activated AMPK and reduced both ER stress and apoptosis in ISO-induced rat heart failure in vivo. We conclude that ISO, via AMPK inactivation, causes aberrant ER stress, cardiomyocyte injury, BNP release, apoptosis, and hence heart failure in vivo, all of which are inhibited by AMPK activation.</abstract><cop>Boston</cop><pub>Springer US</pub><pmid>23620435</pmid><doi>10.1007/s10495-013-0843-5</doi><tpages>11</tpages></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 1360-8185 |
| ispartof | Apoptosis (London), 2013-07, Vol.18 (7), p.800-810 |
| issn | 1360-8185 1573-675X |
| language | eng |
| recordid | cdi_proquest_journals_1356427130 |
| source | MEDLINE; SpringerLink Journals |
| subjects | AMP-Activated Protein Kinases - antagonists & inhibitors AMP-Activated Protein Kinases - deficiency AMP-Activated Protein Kinases - genetics Animals Apoptosis - drug effects Biochemistry Biomedical and Life Sciences Biomedicine Cancer Research Cell Biology Endoplasmic Reticulum - drug effects Endoplasmic Reticulum - genetics Endoplasmic Reticulum - metabolism Endoplasmic Reticulum Stress - drug effects Gene Expression Regulation Heart Failure - chemically induced Heart Failure - enzymology Heart Failure - pathology Heart Failure - prevention & control Inactivation Isoproterenol - adverse effects Male Metformin - pharmacology Mice Mice, Knockout Myocardium - enzymology Myocardium - pathology Myocytes, Cardiac - drug effects Myocytes, Cardiac - enzymology Myocytes, Cardiac - pathology Natriuretic Peptide, Brain - metabolism Oncology Original Paper Phosphorylation Pyrazoles - pharmacology Pyrimidines - pharmacology Rats Rats, Sprague-Dawley Signal Transduction Stress Virology |
| title | Isoproterenol instigates cardiomyocyte apoptosis and heart failure via AMPK inactivation-mediated endoplasmic reticulum stress |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-19T11%3A51%3A13IST&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=Isoproterenol%20instigates%20cardiomyocyte%20apoptosis%20and%20heart%20failure%20via%20AMPK%20inactivation-mediated%20endoplasmic%20reticulum%20stress&rft.jtitle=Apoptosis%20(London)&rft.au=Zhuo,%20Xiao-Zhen&rft.date=2013-07-01&rft.volume=18&rft.issue=7&rft.spage=800&rft.epage=810&rft.pages=800-810&rft.issn=1360-8185&rft.eissn=1573-675X&rft_id=info:doi/10.1007/s10495-013-0843-5&rft_dat=%3Cproquest_cross%3E2983014721%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=1356427130&rft_id=info:pmid/23620435&rfr_iscdi=true |