Attenuation of atrial remodeling by aliskiren via affecting oxidative stress, inflammation and PI3K/Akt signaling pathway
Introduction Atrial fibrillation (AF) is the most common type of arrhythmia. Atrial remodeling is a major factor to the AF substrate. The purpose of the study is to explore whether aliskiren (ALS) has a cardioprotective effect and its potential molecular mechanisms on atrial remodeling. Methods In a...
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| Veröffentlicht in: | Cardiovascular drugs and therapy 2021-06, Vol.35 (3), p.587-598 |
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| description | Introduction
Atrial fibrillation (AF) is the most common type of arrhythmia. Atrial remodeling is a major factor to the AF substrate. The purpose of the study is to explore whether aliskiren (ALS) has a cardioprotective effect and its potential molecular mechanisms on atrial remodeling.
Methods
In acute experiments, dogs were randomly assigned to Sham, Paced and Paced+aliskiren (10 mg kg
−1
) (Paced+ALS) groups, with 7 dogs in each group. Rapid atrial pacing (RAP) was maintained at 600 bpm for 2 h for paced and Paced+ALS groups and atrial effective refractory periods (AERPs), inducibility of AF (AFi) and average duration time (ADT) were measured. In chronic experiments, there were 5 groups: Sham, Sham+ALS, Paced, Paced+ALS and Paced+ALS+PI3K antagonist wortmannin (WM) (70 μg kg
−1
day
−1
). RAP at 500 beats/min was maintained for 2 weeks. Inflammation and oxidative stress indicators were measured by ELISA assay, echocardiogram and pathology were used to assess atrial structural remodeling, phosphatidylinositol 3-hydroxy kinase/protein kinase B (PI3K/Akt) signaling pathways were studied by RT-PCR and western blotting to evaluate whether the cardioprotective effect of ALS works through PI3K/Akt signaling pathway.
Results
The electrophysiological changes were observed after 2-h pacing. The AERP shortened with increased AFi and ADT, which was attenuated by ALS (
P
|
| doi_str_mv | 10.1007/s10557-020-07002-z |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_2407583103</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>2407583103</sourcerecordid><originalsourceid>FETCH-LOGICAL-c375t-64d21c62da8714fdaeaff16be96125671bf0520fbd994c0f8d02c4db198ad7ba3</originalsourceid><addsrcrecordid>eNp9kU1v1DAURS0EokPhD7BAltiwIPT5O1mOKloqKsEC1pYT24PbxBlspzD99bhNAYkFKy_uuedZugi9JPCOAKiTTEAI1QCFBhQAbW4foQ0RijWKcvIYbaCrEaMgj9CznK-glrqufYqOGOWSUik26LAtxcXFlDBHPHtsSgpmxMlNs3VjiDvcH7AZQ74OyUV8Eww23ruh3EXzz2Br88bhXJLL-S0O0Y9mmladiRZ_vmAfT7bXBeewi-ZeuDfl2w9zeI6eeDNm9-LhPUZfz95_Of3QXH46vzjdXjYDU6I0kltKBkmtaRXh3hpX7xPZu04SKqQivQdBwfe26_gAvrVAB2570rXGqt6wY_Rm9e7T_H1xuegp5MGNo4luXrKmHJRoGQFW0df_oFfzkuq3KyUo7SRvBa8UXakhzTkn5_U-hcmkgyag74bR6zC6DqPvh9G3tfTqQb30k7N_Kr-XqABbgVyjuHPp7-3_aH8BKr-a7Q</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>2522964854</pqid></control><display><type>article</type><title>Attenuation of atrial remodeling by aliskiren via affecting oxidative stress, inflammation and PI3K/Akt signaling pathway</title><source>MEDLINE</source><source>SpringerNature Journals</source><creator>Zhao, Zhiqiang ; Li, Ruiling ; Wang, Xinghua ; Li, Jian ; Yuan, Meng ; Liu, Enzhao ; Liu, Tong ; Li, Guangping</creator><creatorcontrib>Zhao, Zhiqiang ; Li, Ruiling ; Wang, Xinghua ; Li, Jian ; Yuan, Meng ; Liu, Enzhao ; Liu, Tong ; Li, Guangping</creatorcontrib><description><![CDATA[Introduction
Atrial fibrillation (AF) is the most common type of arrhythmia. Atrial remodeling is a major factor to the AF substrate. The purpose of the study is to explore whether aliskiren (ALS) has a cardioprotective effect and its potential molecular mechanisms on atrial remodeling.
Methods
In acute experiments, dogs were randomly assigned to Sham, Paced and Paced+aliskiren (10 mg kg
−1
) (Paced+ALS) groups, with 7 dogs in each group. Rapid atrial pacing (RAP) was maintained at 600 bpm for 2 h for paced and Paced+ALS groups and atrial effective refractory periods (AERPs), inducibility of AF (AFi) and average duration time (ADT) were measured. In chronic experiments, there were 5 groups: Sham, Sham+ALS, Paced, Paced+ALS and Paced+ALS+PI3K antagonist wortmannin (WM) (70 μg kg
−1
day
−1
). RAP at 500 beats/min was maintained for 2 weeks. Inflammation and oxidative stress indicators were measured by ELISA assay, echocardiogram and pathology were used to assess atrial structural remodeling, phosphatidylinositol 3-hydroxy kinase/protein kinase B (PI3K/Akt) signaling pathways were studied by RT-PCR and western blotting to evaluate whether the cardioprotective effect of ALS works through PI3K/Akt signaling pathway.
Results
The electrophysiological changes were observed after 2-h pacing. The AERP shortened with increased AFi and ADT, which was attenuated by ALS (
P
< 0.05). After pacing for 2 weeks, oxidative stress and inflammation markers in the Paced group were significantly higher than those in the Sham group (
P
< 0.01) and were reduced by ALS treatment (
P
< 0.01). The reduced level of antioxidant enzymes caused by RAP was also found to be elevated in ALS-treated group (
P
< 0.01). The results of pathology and echocardiography showed that RAP can cause atrial enlargement, fibrosis (
P
< 0.01), and were attenuated in ALS treatment group. The PI3K/Akt signaling pathway were downregulated induced by RAP. ALS could upregulate the PI3K/Akt pathway expression (
P
< 0.05). Furthermore, the cardioprotective effects in structural remodeling of ALS were suppressed by WM.
Conclusions
ALS may offer cardioprotection in RAP-induced atrial remodeling, which may partly be ascribed to its anti-inflammatory and anti-oxidative stress action and the regulation of PI3K/Akt signaling pathway.]]></description><identifier>ISSN: 0920-3206</identifier><identifier>EISSN: 1573-7241</identifier><identifier>DOI: 10.1007/s10557-020-07002-z</identifier><identifier>PMID: 32462265</identifier><language>eng</language><publisher>New York: Springer US</publisher><subject>1-Phosphatidylinositol 3-kinase ; AKT protein ; Amides - pharmacology ; Animals ; Antioxidants ; Arrhythmia ; Atrial Remodeling - drug effects ; Attenuation ; Cardiology ; Dogs ; Echocardiography ; Enlargement ; Enzyme-linked immunosorbent assay ; Female ; Fibrillation ; Fibrosis ; Fumarates - pharmacology ; Inflammation ; Inflammation Mediators - metabolism ; Kinases ; Male ; Medicine ; Medicine & Public Health ; Molecular modelling ; Original Article ; Oxidative stress ; Oxidative Stress - drug effects ; Pathology ; Phosphatidylinositol 3-Kinases - metabolism ; Polymerase chain reaction ; Random Allocation ; Signal transduction ; Signal Transduction - drug effects ; Signaling ; Substrates ; Western blotting ; Wortmannin ; Wortmannin - pharmacology</subject><ispartof>Cardiovascular drugs and therapy, 2021-06, Vol.35 (3), p.587-598</ispartof><rights>Springer Science+Business Media, LLC, part of Springer Nature 2020</rights><rights>Springer Science+Business Media, LLC, part of Springer Nature 2020.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c375t-64d21c62da8714fdaeaff16be96125671bf0520fbd994c0f8d02c4db198ad7ba3</citedby><cites>FETCH-LOGICAL-c375t-64d21c62da8714fdaeaff16be96125671bf0520fbd994c0f8d02c4db198ad7ba3</cites><orcidid>0000-0003-2424-8548</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s10557-020-07002-z$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s10557-020-07002-z$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,780,784,27924,27925,41488,42557,51319</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/32462265$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Zhao, Zhiqiang</creatorcontrib><creatorcontrib>Li, Ruiling</creatorcontrib><creatorcontrib>Wang, Xinghua</creatorcontrib><creatorcontrib>Li, Jian</creatorcontrib><creatorcontrib>Yuan, Meng</creatorcontrib><creatorcontrib>Liu, Enzhao</creatorcontrib><creatorcontrib>Liu, Tong</creatorcontrib><creatorcontrib>Li, Guangping</creatorcontrib><title>Attenuation of atrial remodeling by aliskiren via affecting oxidative stress, inflammation and PI3K/Akt signaling pathway</title><title>Cardiovascular drugs and therapy</title><addtitle>Cardiovasc Drugs Ther</addtitle><addtitle>Cardiovasc Drugs Ther</addtitle><description><![CDATA[Introduction
Atrial fibrillation (AF) is the most common type of arrhythmia. Atrial remodeling is a major factor to the AF substrate. The purpose of the study is to explore whether aliskiren (ALS) has a cardioprotective effect and its potential molecular mechanisms on atrial remodeling.
Methods
In acute experiments, dogs were randomly assigned to Sham, Paced and Paced+aliskiren (10 mg kg
−1
) (Paced+ALS) groups, with 7 dogs in each group. Rapid atrial pacing (RAP) was maintained at 600 bpm for 2 h for paced and Paced+ALS groups and atrial effective refractory periods (AERPs), inducibility of AF (AFi) and average duration time (ADT) were measured. In chronic experiments, there were 5 groups: Sham, Sham+ALS, Paced, Paced+ALS and Paced+ALS+PI3K antagonist wortmannin (WM) (70 μg kg
−1
day
−1
). RAP at 500 beats/min was maintained for 2 weeks. Inflammation and oxidative stress indicators were measured by ELISA assay, echocardiogram and pathology were used to assess atrial structural remodeling, phosphatidylinositol 3-hydroxy kinase/protein kinase B (PI3K/Akt) signaling pathways were studied by RT-PCR and western blotting to evaluate whether the cardioprotective effect of ALS works through PI3K/Akt signaling pathway.
Results
The electrophysiological changes were observed after 2-h pacing. The AERP shortened with increased AFi and ADT, which was attenuated by ALS (
P
< 0.05). After pacing for 2 weeks, oxidative stress and inflammation markers in the Paced group were significantly higher than those in the Sham group (
P
< 0.01) and were reduced by ALS treatment (
P
< 0.01). The reduced level of antioxidant enzymes caused by RAP was also found to be elevated in ALS-treated group (
P
< 0.01). The results of pathology and echocardiography showed that RAP can cause atrial enlargement, fibrosis (
P
< 0.01), and were attenuated in ALS treatment group. The PI3K/Akt signaling pathway were downregulated induced by RAP. ALS could upregulate the PI3K/Akt pathway expression (
P
< 0.05). Furthermore, the cardioprotective effects in structural remodeling of ALS were suppressed by WM.
Conclusions
ALS may offer cardioprotection in RAP-induced atrial remodeling, which may partly be ascribed to its anti-inflammatory and anti-oxidative stress action and the regulation of PI3K/Akt signaling pathway.]]></description><subject>1-Phosphatidylinositol 3-kinase</subject><subject>AKT protein</subject><subject>Amides - pharmacology</subject><subject>Animals</subject><subject>Antioxidants</subject><subject>Arrhythmia</subject><subject>Atrial Remodeling - drug effects</subject><subject>Attenuation</subject><subject>Cardiology</subject><subject>Dogs</subject><subject>Echocardiography</subject><subject>Enlargement</subject><subject>Enzyme-linked immunosorbent assay</subject><subject>Female</subject><subject>Fibrillation</subject><subject>Fibrosis</subject><subject>Fumarates - pharmacology</subject><subject>Inflammation</subject><subject>Inflammation Mediators - metabolism</subject><subject>Kinases</subject><subject>Male</subject><subject>Medicine</subject><subject>Medicine & Public Health</subject><subject>Molecular modelling</subject><subject>Original Article</subject><subject>Oxidative stress</subject><subject>Oxidative Stress - drug effects</subject><subject>Pathology</subject><subject>Phosphatidylinositol 3-Kinases - metabolism</subject><subject>Polymerase chain reaction</subject><subject>Random Allocation</subject><subject>Signal transduction</subject><subject>Signal Transduction - drug effects</subject><subject>Signaling</subject><subject>Substrates</subject><subject>Western blotting</subject><subject>Wortmannin</subject><subject>Wortmannin - pharmacology</subject><issn>0920-3206</issn><issn>1573-7241</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2021</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><recordid>eNp9kU1v1DAURS0EokPhD7BAltiwIPT5O1mOKloqKsEC1pYT24PbxBlspzD99bhNAYkFKy_uuedZugi9JPCOAKiTTEAI1QCFBhQAbW4foQ0RijWKcvIYbaCrEaMgj9CznK-glrqufYqOGOWSUik26LAtxcXFlDBHPHtsSgpmxMlNs3VjiDvcH7AZQ74OyUV8Eww23ruh3EXzz2Br88bhXJLL-S0O0Y9mmladiRZ_vmAfT7bXBeewi-ZeuDfl2w9zeI6eeDNm9-LhPUZfz95_Of3QXH46vzjdXjYDU6I0kltKBkmtaRXh3hpX7xPZu04SKqQivQdBwfe26_gAvrVAB2570rXGqt6wY_Rm9e7T_H1xuegp5MGNo4luXrKmHJRoGQFW0df_oFfzkuq3KyUo7SRvBa8UXakhzTkn5_U-hcmkgyag74bR6zC6DqPvh9G3tfTqQb30k7N_Kr-XqABbgVyjuHPp7-3_aH8BKr-a7Q</recordid><startdate>20210601</startdate><enddate>20210601</enddate><creator>Zhao, Zhiqiang</creator><creator>Li, Ruiling</creator><creator>Wang, Xinghua</creator><creator>Li, Jian</creator><creator>Yuan, Meng</creator><creator>Liu, Enzhao</creator><creator>Liu, Tong</creator><creator>Li, Guangping</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>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8FD</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>M7Z</scope><scope>P64</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope><orcidid>https://orcid.org/0000-0003-2424-8548</orcidid></search><sort><creationdate>20210601</creationdate><title>Attenuation of atrial remodeling by aliskiren via affecting oxidative stress, inflammation and PI3K/Akt signaling pathway</title><author>Zhao, Zhiqiang ; Li, Ruiling ; Wang, Xinghua ; Li, Jian ; Yuan, Meng ; Liu, Enzhao ; Liu, Tong ; Li, Guangping</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c375t-64d21c62da8714fdaeaff16be96125671bf0520fbd994c0f8d02c4db198ad7ba3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2021</creationdate><topic>1-Phosphatidylinositol 3-kinase</topic><topic>AKT protein</topic><topic>Amides - pharmacology</topic><topic>Animals</topic><topic>Antioxidants</topic><topic>Arrhythmia</topic><topic>Atrial Remodeling - drug effects</topic><topic>Attenuation</topic><topic>Cardiology</topic><topic>Dogs</topic><topic>Echocardiography</topic><topic>Enlargement</topic><topic>Enzyme-linked immunosorbent assay</topic><topic>Female</topic><topic>Fibrillation</topic><topic>Fibrosis</topic><topic>Fumarates - pharmacology</topic><topic>Inflammation</topic><topic>Inflammation Mediators - metabolism</topic><topic>Kinases</topic><topic>Male</topic><topic>Medicine</topic><topic>Medicine & Public Health</topic><topic>Molecular modelling</topic><topic>Original Article</topic><topic>Oxidative stress</topic><topic>Oxidative Stress - drug effects</topic><topic>Pathology</topic><topic>Phosphatidylinositol 3-Kinases - metabolism</topic><topic>Polymerase chain reaction</topic><topic>Random Allocation</topic><topic>Signal transduction</topic><topic>Signal Transduction - drug effects</topic><topic>Signaling</topic><topic>Substrates</topic><topic>Western blotting</topic><topic>Wortmannin</topic><topic>Wortmannin - pharmacology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Zhao, Zhiqiang</creatorcontrib><creatorcontrib>Li, Ruiling</creatorcontrib><creatorcontrib>Wang, Xinghua</creatorcontrib><creatorcontrib>Li, Jian</creatorcontrib><creatorcontrib>Yuan, Meng</creatorcontrib><creatorcontrib>Liu, Enzhao</creatorcontrib><creatorcontrib>Liu, Tong</creatorcontrib><creatorcontrib>Li, Guangping</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>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Technology Research Database</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 Central UK/Ireland</collection><collection>Proquest Central</collection><collection>ProQuest One Community College</collection><collection>Engineering Research Database</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Biochemistry Abstracts 1</collection><collection>Biotechnology and BioEngineering Abstracts</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>MEDLINE - Academic</collection><jtitle>Cardiovascular drugs and therapy</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Zhao, Zhiqiang</au><au>Li, Ruiling</au><au>Wang, Xinghua</au><au>Li, Jian</au><au>Yuan, Meng</au><au>Liu, Enzhao</au><au>Liu, Tong</au><au>Li, Guangping</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Attenuation of atrial remodeling by aliskiren via affecting oxidative stress, inflammation and PI3K/Akt signaling pathway</atitle><jtitle>Cardiovascular drugs and therapy</jtitle><stitle>Cardiovasc Drugs Ther</stitle><addtitle>Cardiovasc Drugs Ther</addtitle><date>2021-06-01</date><risdate>2021</risdate><volume>35</volume><issue>3</issue><spage>587</spage><epage>598</epage><pages>587-598</pages><issn>0920-3206</issn><eissn>1573-7241</eissn><abstract><![CDATA[Introduction
Atrial fibrillation (AF) is the most common type of arrhythmia. Atrial remodeling is a major factor to the AF substrate. The purpose of the study is to explore whether aliskiren (ALS) has a cardioprotective effect and its potential molecular mechanisms on atrial remodeling.
Methods
In acute experiments, dogs were randomly assigned to Sham, Paced and Paced+aliskiren (10 mg kg
−1
) (Paced+ALS) groups, with 7 dogs in each group. Rapid atrial pacing (RAP) was maintained at 600 bpm for 2 h for paced and Paced+ALS groups and atrial effective refractory periods (AERPs), inducibility of AF (AFi) and average duration time (ADT) were measured. In chronic experiments, there were 5 groups: Sham, Sham+ALS, Paced, Paced+ALS and Paced+ALS+PI3K antagonist wortmannin (WM) (70 μg kg
−1
day
−1
). RAP at 500 beats/min was maintained for 2 weeks. Inflammation and oxidative stress indicators were measured by ELISA assay, echocardiogram and pathology were used to assess atrial structural remodeling, phosphatidylinositol 3-hydroxy kinase/protein kinase B (PI3K/Akt) signaling pathways were studied by RT-PCR and western blotting to evaluate whether the cardioprotective effect of ALS works through PI3K/Akt signaling pathway.
Results
The electrophysiological changes were observed after 2-h pacing. The AERP shortened with increased AFi and ADT, which was attenuated by ALS (
P
< 0.05). After pacing for 2 weeks, oxidative stress and inflammation markers in the Paced group were significantly higher than those in the Sham group (
P
< 0.01) and were reduced by ALS treatment (
P
< 0.01). The reduced level of antioxidant enzymes caused by RAP was also found to be elevated in ALS-treated group (
P
< 0.01). The results of pathology and echocardiography showed that RAP can cause atrial enlargement, fibrosis (
P
< 0.01), and were attenuated in ALS treatment group. The PI3K/Akt signaling pathway were downregulated induced by RAP. ALS could upregulate the PI3K/Akt pathway expression (
P
< 0.05). Furthermore, the cardioprotective effects in structural remodeling of ALS were suppressed by WM.
Conclusions
ALS may offer cardioprotection in RAP-induced atrial remodeling, which may partly be ascribed to its anti-inflammatory and anti-oxidative stress action and the regulation of PI3K/Akt signaling pathway.]]></abstract><cop>New York</cop><pub>Springer US</pub><pmid>32462265</pmid><doi>10.1007/s10557-020-07002-z</doi><tpages>12</tpages><orcidid>https://orcid.org/0000-0003-2424-8548</orcidid></addata></record> |
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| ispartof | Cardiovascular drugs and therapy, 2021-06, Vol.35 (3), p.587-598 |
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| source | MEDLINE; SpringerNature Journals |
| subjects | 1-Phosphatidylinositol 3-kinase AKT protein Amides - pharmacology Animals Antioxidants Arrhythmia Atrial Remodeling - drug effects Attenuation Cardiology Dogs Echocardiography Enlargement Enzyme-linked immunosorbent assay Female Fibrillation Fibrosis Fumarates - pharmacology Inflammation Inflammation Mediators - metabolism Kinases Male Medicine Medicine & Public Health Molecular modelling Original Article Oxidative stress Oxidative Stress - drug effects Pathology Phosphatidylinositol 3-Kinases - metabolism Polymerase chain reaction Random Allocation Signal transduction Signal Transduction - drug effects Signaling Substrates Western blotting Wortmannin Wortmannin - pharmacology |
| title | Attenuation of atrial remodeling by aliskiren via affecting oxidative stress, inflammation and PI3K/Akt signaling pathway |
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