Fetal cardiomyocyte phenotype, ketone body metabolism, and mitochondrial dysfunction in the pathology of atrial fibrillation
Atrial fibrillation (AF) is the most common cardiac arrhythmia diagnosed in clinical practice. Even though hypertension, congestive heart failure, pulmonary disease, and coronary artery disease are the potential risk factors for AF, the underlying molecular pathology is largely unknown. The reversio...
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| Veröffentlicht in: | Molecular and cellular biochemistry 2021-02, Vol.476 (2), p.1165-1178 |
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| creator | Brown, Sean M. Larsen, Nicholas K. Thankam, Finosh G. Agrawal, Devendra K |
| description | Atrial fibrillation (AF) is the most common cardiac arrhythmia diagnosed in clinical practice. Even though hypertension, congestive heart failure, pulmonary disease, and coronary artery disease are the potential risk factors for AF, the underlying molecular pathology is largely unknown. The reversion of the mature cardiomyocytes to fetal phenotype, impaired ketone body metabolism, mitochondrial dysfunction, and the cellular effect of reactive oxygen species (ROS) are the major underlying biochemical events associated with the molecular pathology of AF. On this background, the present manuscript sheds light into these biochemical events in regard to the metabolic derangements in cardiomyocyte leading to AF, especially with respect to structural, contractile, and electrophysiological properties. In addition, the article critically reviews the current understanding, potential demerits, and translational strategies in the management of AF. |
| doi_str_mv | 10.1007/s11010-020-03980-8 |
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Even though hypertension, congestive heart failure, pulmonary disease, and coronary artery disease are the potential risk factors for AF, the underlying molecular pathology is largely unknown. The reversion of the mature cardiomyocytes to fetal phenotype, impaired ketone body metabolism, mitochondrial dysfunction, and the cellular effect of reactive oxygen species (ROS) are the major underlying biochemical events associated with the molecular pathology of AF. On this background, the present manuscript sheds light into these biochemical events in regard to the metabolic derangements in cardiomyocyte leading to AF, especially with respect to structural, contractile, and electrophysiological properties. In addition, the article critically reviews the current understanding, potential demerits, and translational strategies in the management of AF.</description><identifier>ISSN: 0300-8177</identifier><identifier>EISSN: 1573-4919</identifier><identifier>DOI: 10.1007/s11010-020-03980-8</identifier><identifier>PMID: 33188453</identifier><language>eng</language><publisher>New York: Springer US</publisher><subject>Amino acids ; Apixaban ; Arrhythmia ; Atrial fibrillation ; Atrial Fibrillation - etiology ; Atrial Fibrillation - metabolism ; Atrial Fibrillation - pathology ; Biochemistry ; Biomedical and Life Sciences ; Cardiac arrhythmia ; Cardiology ; Cardiomyocytes ; Cardiovascular disease ; Clopidogrel ; Congestive heart failure ; Coronary artery ; Coronary artery disease ; Coronary heart disease ; Fetus - physiopathology ; Fetuses ; Fibrillation ; Genetic aspects ; Heart ; Humans ; Hypertension ; Ketone Bodies - metabolism ; Ketones ; Life Sciences ; Lung diseases ; Medical Biochemistry ; Metabolism ; Mitochondria ; Mitochondria - metabolism ; Mitochondria - pathology ; Muscle contraction ; Myocytes, Cardiac - metabolism ; Myocytes, Cardiac - pathology ; Oncology ; Pathology ; Phenotype ; Phenotypes ; Physiological aspects ; Pulmonary artery ; Reactive oxygen species ; Reactive Oxygen Species - metabolism ; Reversion ; Risk analysis ; Risk factors ; Rivaroxaban</subject><ispartof>Molecular and cellular biochemistry, 2021-02, Vol.476 (2), p.1165-1178</ispartof><rights>Springer Science+Business Media, LLC, part of Springer Nature 2020</rights><rights>COPYRIGHT 2020 Springer</rights><rights>Springer Science+Business Media, LLC, part of Springer Nature 2020.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c541t-488b99515b72da75300af9c52dc44c61ac6863dc95bb5c292689cfe73bddce3d3</citedby><cites>FETCH-LOGICAL-c541t-488b99515b72da75300af9c52dc44c61ac6863dc95bb5c292689cfe73bddce3d3</cites><orcidid>0000-0001-5445-0013</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/s11010-020-03980-8$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s11010-020-03980-8$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>230,314,780,784,885,27915,27916,41479,42548,51310</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/33188453$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Brown, Sean M.</creatorcontrib><creatorcontrib>Larsen, Nicholas K.</creatorcontrib><creatorcontrib>Thankam, Finosh G.</creatorcontrib><creatorcontrib>Agrawal, Devendra K</creatorcontrib><title>Fetal cardiomyocyte phenotype, ketone body metabolism, and mitochondrial dysfunction in the pathology of atrial fibrillation</title><title>Molecular and cellular biochemistry</title><addtitle>Mol Cell Biochem</addtitle><addtitle>Mol Cell Biochem</addtitle><description>Atrial fibrillation (AF) is the most common cardiac arrhythmia diagnosed in clinical practice. Even though hypertension, congestive heart failure, pulmonary disease, and coronary artery disease are the potential risk factors for AF, the underlying molecular pathology is largely unknown. The reversion of the mature cardiomyocytes to fetal phenotype, impaired ketone body metabolism, mitochondrial dysfunction, and the cellular effect of reactive oxygen species (ROS) are the major underlying biochemical events associated with the molecular pathology of AF. On this background, the present manuscript sheds light into these biochemical events in regard to the metabolic derangements in cardiomyocyte leading to AF, especially with respect to structural, contractile, and electrophysiological properties. In addition, the article critically reviews the current understanding, potential demerits, and translational strategies in the management of AF.</description><subject>Amino acids</subject><subject>Apixaban</subject><subject>Arrhythmia</subject><subject>Atrial fibrillation</subject><subject>Atrial Fibrillation - etiology</subject><subject>Atrial Fibrillation - metabolism</subject><subject>Atrial Fibrillation - pathology</subject><subject>Biochemistry</subject><subject>Biomedical and Life Sciences</subject><subject>Cardiac arrhythmia</subject><subject>Cardiology</subject><subject>Cardiomyocytes</subject><subject>Cardiovascular disease</subject><subject>Clopidogrel</subject><subject>Congestive heart failure</subject><subject>Coronary artery</subject><subject>Coronary artery disease</subject><subject>Coronary heart disease</subject><subject>Fetus - physiopathology</subject><subject>Fetuses</subject><subject>Fibrillation</subject><subject>Genetic aspects</subject><subject>Heart</subject><subject>Humans</subject><subject>Hypertension</subject><subject>Ketone Bodies - metabolism</subject><subject>Ketones</subject><subject>Life Sciences</subject><subject>Lung diseases</subject><subject>Medical Biochemistry</subject><subject>Metabolism</subject><subject>Mitochondria</subject><subject>Mitochondria - metabolism</subject><subject>Mitochondria - pathology</subject><subject>Muscle contraction</subject><subject>Myocytes, Cardiac - metabolism</subject><subject>Myocytes, Cardiac - pathology</subject><subject>Oncology</subject><subject>Pathology</subject><subject>Phenotype</subject><subject>Phenotypes</subject><subject>Physiological aspects</subject><subject>Pulmonary artery</subject><subject>Reactive oxygen species</subject><subject>Reactive Oxygen Species - metabolism</subject><subject>Reversion</subject><subject>Risk analysis</subject><subject>Risk factors</subject><subject>Rivaroxaban</subject><issn>0300-8177</issn><issn>1573-4919</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2021</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>eNp9kk9rFTEUxQdR7Gv1C7iQgBsXnZpMJn9mI5TSqlBwo-uQSTJvUmeSZ5IRBvzw3tdXWysiIQTu_d0TTnKq6hXBZwRj8S4TggmucQObdhLX8km1IUzQuu1I97TaYIqhSIQ4qo5zvsFAY0KeV0eUEilbRjfVzytX9ISMTtbHeY1mLQ7tRhdiWXfuFH1zJQaH-mhXNAPax8nn-RTpYNHsSzRjDDZ5kLBrHpZgio8B-YDKCDq6jHGK2xXFAelyiw2-T36a9J57UT0b9JTdy7vzpPp6dfnl4mN9_fnDp4vz69qwlpS6lbLvOkZYLxqrBQNXeugMa6xpW8OJNlxyak3H-p6Zpmu47MzgBO2tNY5aelK9P-juln52UAsl6Untkp91WlXUXj3uBD-qbfyhhBSS8gYE3t4JpPh9cbmo2WfjwEZwccmqaTkWnErOAX3zF3oTlxTAHlByDzHKHqitnpzyYYhwr9mLqnPOCGUdEwKos39QsKybvYF_GTzUHw00hwGTYs7JDfceCVb7zKhDZhRkRt1mRkkYev3n69yP_A4JAPQAZGiFrUsPlv4j-wsT286i</recordid><startdate>20210201</startdate><enddate>20210201</enddate><creator>Brown, Sean M.</creator><creator>Larsen, Nicholas K.</creator><creator>Thankam, Finosh G.</creator><creator>Agrawal, Devendra K</creator><general>Springer US</general><general>Springer</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>7T5</scope><scope>7T7</scope><scope>7TK</scope><scope>7TM</scope><scope>7TO</scope><scope>7U9</scope><scope>7X7</scope><scope>7XB</scope><scope>88A</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>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>FR3</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>M2P</scope><scope>M7N</scope><scope>M7P</scope><scope>P64</scope><scope>PQEST</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/0000-0001-5445-0013</orcidid></search><sort><creationdate>20210201</creationdate><title>Fetal cardiomyocyte phenotype, ketone body metabolism, and mitochondrial dysfunction in the pathology of atrial fibrillation</title><author>Brown, Sean M. ; Larsen, Nicholas K. ; Thankam, Finosh G. ; Agrawal, Devendra K</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c541t-488b99515b72da75300af9c52dc44c61ac6863dc95bb5c292689cfe73bddce3d3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2021</creationdate><topic>Amino acids</topic><topic>Apixaban</topic><topic>Arrhythmia</topic><topic>Atrial fibrillation</topic><topic>Atrial Fibrillation - etiology</topic><topic>Atrial Fibrillation - metabolism</topic><topic>Atrial Fibrillation - pathology</topic><topic>Biochemistry</topic><topic>Biomedical and Life Sciences</topic><topic>Cardiac arrhythmia</topic><topic>Cardiology</topic><topic>Cardiomyocytes</topic><topic>Cardiovascular disease</topic><topic>Clopidogrel</topic><topic>Congestive heart failure</topic><topic>Coronary artery</topic><topic>Coronary artery disease</topic><topic>Coronary heart disease</topic><topic>Fetus - physiopathology</topic><topic>Fetuses</topic><topic>Fibrillation</topic><topic>Genetic aspects</topic><topic>Heart</topic><topic>Humans</topic><topic>Hypertension</topic><topic>Ketone Bodies - metabolism</topic><topic>Ketones</topic><topic>Life Sciences</topic><topic>Lung diseases</topic><topic>Medical Biochemistry</topic><topic>Metabolism</topic><topic>Mitochondria</topic><topic>Mitochondria - metabolism</topic><topic>Mitochondria - pathology</topic><topic>Muscle contraction</topic><topic>Myocytes, Cardiac - 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Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Molecular and cellular biochemistry</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Brown, Sean M.</au><au>Larsen, Nicholas K.</au><au>Thankam, Finosh G.</au><au>Agrawal, Devendra K</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Fetal cardiomyocyte phenotype, ketone body metabolism, and mitochondrial dysfunction in the pathology of atrial fibrillation</atitle><jtitle>Molecular and cellular biochemistry</jtitle><stitle>Mol Cell Biochem</stitle><addtitle>Mol Cell Biochem</addtitle><date>2021-02-01</date><risdate>2021</risdate><volume>476</volume><issue>2</issue><spage>1165</spage><epage>1178</epage><pages>1165-1178</pages><issn>0300-8177</issn><eissn>1573-4919</eissn><abstract>Atrial fibrillation (AF) is the most common cardiac arrhythmia diagnosed in clinical practice. Even though hypertension, congestive heart failure, pulmonary disease, and coronary artery disease are the potential risk factors for AF, the underlying molecular pathology is largely unknown. The reversion of the mature cardiomyocytes to fetal phenotype, impaired ketone body metabolism, mitochondrial dysfunction, and the cellular effect of reactive oxygen species (ROS) are the major underlying biochemical events associated with the molecular pathology of AF. On this background, the present manuscript sheds light into these biochemical events in regard to the metabolic derangements in cardiomyocyte leading to AF, especially with respect to structural, contractile, and electrophysiological properties. In addition, the article critically reviews the current understanding, potential demerits, and translational strategies in the management of AF.</abstract><cop>New York</cop><pub>Springer US</pub><pmid>33188453</pmid><doi>10.1007/s11010-020-03980-8</doi><tpages>14</tpages><orcidid>https://orcid.org/0000-0001-5445-0013</orcidid><oa>free_for_read</oa></addata></record> |
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| subjects | Amino acids Apixaban Arrhythmia Atrial fibrillation Atrial Fibrillation - etiology Atrial Fibrillation - metabolism Atrial Fibrillation - pathology Biochemistry Biomedical and Life Sciences Cardiac arrhythmia Cardiology Cardiomyocytes Cardiovascular disease Clopidogrel Congestive heart failure Coronary artery Coronary artery disease Coronary heart disease Fetus - physiopathology Fetuses Fibrillation Genetic aspects Heart Humans Hypertension Ketone Bodies - metabolism Ketones Life Sciences Lung diseases Medical Biochemistry Metabolism Mitochondria Mitochondria - metabolism Mitochondria - pathology Muscle contraction Myocytes, Cardiac - metabolism Myocytes, Cardiac - pathology Oncology Pathology Phenotype Phenotypes Physiological aspects Pulmonary artery Reactive oxygen species Reactive Oxygen Species - metabolism Reversion Risk analysis Risk factors Rivaroxaban |
| title | Fetal cardiomyocyte phenotype, ketone body metabolism, and mitochondrial dysfunction in the pathology of atrial fibrillation |
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