Indirect epigenetic testing identifies a diagnostic signature of cardiomyocyte DNA methylation in heart failure
Precision-based molecular phenotyping of heart failure must overcome limited access to cardiac tissue. Although epigenetic alterations have been found to underlie pathological cardiac gene dysregulation, the clinical utility of myocardial epigenomics remains narrow owing to limited clinical access t...
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| Veröffentlicht in: | Basic research in cardiology 2023-03, Vol.118 (1), p.9-9, Article 9 |
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| creator | Oeing, Christian U. Pepin, Mark E. Saul, Kerstin B. Agircan, Ayça Seyhan Assenov, Yassen Merkel, Tobias S. Sedaghat-Hamedani, Farbod Weis, Tanja Meder, Benjamin Guan, Kaomei Plass, Christoph Weichenhan, Dieter Siede, Dominik Backs, Johannes |
| description | Precision-based molecular phenotyping of heart failure must overcome limited access to cardiac tissue. Although epigenetic alterations have been found to underlie pathological cardiac gene dysregulation, the clinical utility of myocardial epigenomics remains narrow owing to limited clinical access to tissue. Therefore, the current study determined whether patient plasma confers indirect phenotypic, transcriptional, and/or epigenetic alterations to ex vivo cardiomyocytes to mirror the failing human myocardium. Neonatal rat ventricular myocytes (NRVMs) and single-origin human induced pluripotent stem cell-derived cardiomyocytes (
hiPSC-CMs
) and were treated with blood plasma samples from patients with dilated cardiomyopathy (DCM) and donor subjects lacking history of cardiovascular disease. Following plasma treatments, NRVMs and
hiPSC-CMs
underwent significant hypertrophy relative to non-failing controls, as determined via automated high-content screening. Array-based DNA methylation analysis of plasma-treated
hiPSC-CMs
and cardiac biopsies uncovered robust, and conserved, alterations in cardiac DNA methylation, from which 100 sites were validated using an independent cohort. Among the CpG sites identified, hypo-methylation of the
ATG
promoter was identified as a diagnostic marker of HF, wherein cg03800765 methylation (AUC = 0.986,
P
|
| doi_str_mv | 10.1007/s00395-022-00954-3 |
| format | Article |
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hiPSC-CMs
) and were treated with blood plasma samples from patients with dilated cardiomyopathy (DCM) and donor subjects lacking history of cardiovascular disease. Following plasma treatments, NRVMs and
hiPSC-CMs
underwent significant hypertrophy relative to non-failing controls, as determined via automated high-content screening. Array-based DNA methylation analysis of plasma-treated
hiPSC-CMs
and cardiac biopsies uncovered robust, and conserved, alterations in cardiac DNA methylation, from which 100 sites were validated using an independent cohort. Among the CpG sites identified, hypo-methylation of the
ATG
promoter was identified as a diagnostic marker of HF, wherein cg03800765 methylation (AUC = 0.986,
P
< 0.0001) was found to out-perform circulating NT-proBNP levels in differentiating heart failure. Taken together, these findings support a novel approach of indirect epigenetic testing in human HF.</description><identifier>ISSN: 1435-1803</identifier><identifier>ISSN: 0300-8428</identifier><identifier>EISSN: 1435-1803</identifier><identifier>DOI: 10.1007/s00395-022-00954-3</identifier><identifier>PMID: 36939901</identifier><language>eng</language><publisher>Berlin/Heidelberg: Springer Berlin Heidelberg</publisher><subject>Animals ; Biopsy ; Blood plasma ; Cardiac muscle ; Cardiology ; Cardiomyocytes ; Cardiomyopathy ; Cardiovascular diseases ; Congestive heart failure ; CpG islands ; Deoxyribonucleic acid ; Diagnostic systems ; Dilated cardiomyopathy ; DNA ; DNA Methylation ; Epigenesis, Genetic ; Epigenetics ; Epigenomics ; Heart failure ; Heart Failure - diagnosis ; Heart Failure - genetics ; Heart Failure - pathology ; Humans ; Hypertrophy ; Induced Pluripotent Stem Cells ; Medicine ; Medicine & Public Health ; Myocardium ; Myocytes ; Myocytes, Cardiac - pathology ; Neonates ; Original Contribution ; Phenotyping ; Plasma ; Pluripotency ; Rats ; Stem cells ; Ventricle</subject><ispartof>Basic research in cardiology, 2023-03, Vol.118 (1), p.9-9, Article 9</ispartof><rights>The Author(s) 2023</rights><rights>2023. The Author(s).</rights><rights>The Author(s) 2023. 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-c475t-8dfb5504615536b3891ff4ae8a955d8f75bec1d79f58a4518706590c0b53f7883</citedby><cites>FETCH-LOGICAL-c475t-8dfb5504615536b3891ff4ae8a955d8f75bec1d79f58a4518706590c0b53f7883</cites><orcidid>0000-0002-2322-2699</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/s00395-022-00954-3$$EPDF$$P50$$Gspringer$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s00395-022-00954-3$$EHTML$$P50$$Gspringer$$Hfree_for_read</linktohtml><link.rule.ids>230,314,776,780,881,27901,27902,41464,42533,51294</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/36939901$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Oeing, Christian U.</creatorcontrib><creatorcontrib>Pepin, Mark E.</creatorcontrib><creatorcontrib>Saul, Kerstin B.</creatorcontrib><creatorcontrib>Agircan, Ayça Seyhan</creatorcontrib><creatorcontrib>Assenov, Yassen</creatorcontrib><creatorcontrib>Merkel, Tobias S.</creatorcontrib><creatorcontrib>Sedaghat-Hamedani, Farbod</creatorcontrib><creatorcontrib>Weis, Tanja</creatorcontrib><creatorcontrib>Meder, Benjamin</creatorcontrib><creatorcontrib>Guan, Kaomei</creatorcontrib><creatorcontrib>Plass, Christoph</creatorcontrib><creatorcontrib>Weichenhan, Dieter</creatorcontrib><creatorcontrib>Siede, Dominik</creatorcontrib><creatorcontrib>Backs, Johannes</creatorcontrib><title>Indirect epigenetic testing identifies a diagnostic signature of cardiomyocyte DNA methylation in heart failure</title><title>Basic research in cardiology</title><addtitle>Basic Res Cardiol</addtitle><addtitle>Basic Res Cardiol</addtitle><description>Precision-based molecular phenotyping of heart failure must overcome limited access to cardiac tissue. Although epigenetic alterations have been found to underlie pathological cardiac gene dysregulation, the clinical utility of myocardial epigenomics remains narrow owing to limited clinical access to tissue. Therefore, the current study determined whether patient plasma confers indirect phenotypic, transcriptional, and/or epigenetic alterations to ex vivo cardiomyocytes to mirror the failing human myocardium. Neonatal rat ventricular myocytes (NRVMs) and single-origin human induced pluripotent stem cell-derived cardiomyocytes (
hiPSC-CMs
) and were treated with blood plasma samples from patients with dilated cardiomyopathy (DCM) and donor subjects lacking history of cardiovascular disease. Following plasma treatments, NRVMs and
hiPSC-CMs
underwent significant hypertrophy relative to non-failing controls, as determined via automated high-content screening. Array-based DNA methylation analysis of plasma-treated
hiPSC-CMs
and cardiac biopsies uncovered robust, and conserved, alterations in cardiac DNA methylation, from which 100 sites were validated using an independent cohort. Among the CpG sites identified, hypo-methylation of the
ATG
promoter was identified as a diagnostic marker of HF, wherein cg03800765 methylation (AUC = 0.986,
P
< 0.0001) was found to out-perform circulating NT-proBNP levels in differentiating heart failure. Taken together, these findings support a novel approach of indirect epigenetic testing in human HF.</description><subject>Animals</subject><subject>Biopsy</subject><subject>Blood plasma</subject><subject>Cardiac muscle</subject><subject>Cardiology</subject><subject>Cardiomyocytes</subject><subject>Cardiomyopathy</subject><subject>Cardiovascular diseases</subject><subject>Congestive heart failure</subject><subject>CpG islands</subject><subject>Deoxyribonucleic acid</subject><subject>Diagnostic systems</subject><subject>Dilated cardiomyopathy</subject><subject>DNA</subject><subject>DNA Methylation</subject><subject>Epigenesis, Genetic</subject><subject>Epigenetics</subject><subject>Epigenomics</subject><subject>Heart failure</subject><subject>Heart Failure - diagnosis</subject><subject>Heart Failure - genetics</subject><subject>Heart Failure - pathology</subject><subject>Humans</subject><subject>Hypertrophy</subject><subject>Induced Pluripotent Stem Cells</subject><subject>Medicine</subject><subject>Medicine & Public Health</subject><subject>Myocardium</subject><subject>Myocytes</subject><subject>Myocytes, Cardiac - pathology</subject><subject>Neonates</subject><subject>Original Contribution</subject><subject>Phenotyping</subject><subject>Plasma</subject><subject>Pluripotency</subject><subject>Rats</subject><subject>Stem cells</subject><subject>Ventricle</subject><issn>1435-1803</issn><issn>0300-8428</issn><issn>1435-1803</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2023</creationdate><recordtype>article</recordtype><sourceid>C6C</sourceid><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><recordid>eNp9UU1vFSEUJUZja_UPuDAkbtyMwjAwsDJNtdqkaTe6JgxzmUczA09gTN6_l9dXa-2iK0ju-bjnHoTeUvKREtJ_yoQwxRvStg0hincNe4aOacd4QyVhzx_8j9CrnG8IoZ0Q9CU6YkIxpQg9RvEijD6BLRi2foIAxVtcIBcfJuxHCMU7DxkbPHozhZj38-ynYMqaAEeHrUmjj8su2l0B_OXqFC9QNrvZFB8D9gFvwKSCnfFzZbxGL5yZM7y5e0_Qz_OvP86-N5fX3y7OTi8b2_W8NHJ0A-ekE5RzJgYmFXWuMyCN4nyUrucDWDr2ynFpOk5lTwRXxJKBM9dLyU7Q54Pudh0WGG0Nksyst8kvJu10NF7_Pwl-o6f4W9fLtr3gtCp8uFNI8ddaL6IXny3MswkQ16zbatMr0bE99P0j6E1cU6j5dKtISwXnnaio9oCyKeacwN1vQ8netteHQnUtVN8WqlklvXuY457yt8EKYAdArqMwQfrn_YTsH-05rUA</recordid><startdate>20230320</startdate><enddate>20230320</enddate><creator>Oeing, Christian U.</creator><creator>Pepin, Mark E.</creator><creator>Saul, Kerstin B.</creator><creator>Agircan, Ayça Seyhan</creator><creator>Assenov, Yassen</creator><creator>Merkel, Tobias S.</creator><creator>Sedaghat-Hamedani, Farbod</creator><creator>Weis, Tanja</creator><creator>Meder, Benjamin</creator><creator>Guan, Kaomei</creator><creator>Plass, Christoph</creator><creator>Weichenhan, Dieter</creator><creator>Siede, Dominik</creator><creator>Backs, Johannes</creator><general>Springer Berlin Heidelberg</general><general>Springer Nature B.V</general><scope>C6C</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>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>7X8</scope><scope>5PM</scope><orcidid>https://orcid.org/0000-0002-2322-2699</orcidid></search><sort><creationdate>20230320</creationdate><title>Indirect epigenetic testing identifies a diagnostic signature of cardiomyocyte DNA methylation in heart failure</title><author>Oeing, Christian U. ; Pepin, Mark E. ; Saul, Kerstin B. ; Agircan, Ayça Seyhan ; Assenov, Yassen ; Merkel, Tobias S. ; Sedaghat-Hamedani, Farbod ; Weis, Tanja ; Meder, Benjamin ; Guan, Kaomei ; Plass, Christoph ; Weichenhan, Dieter ; Siede, Dominik ; Backs, Johannes</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c475t-8dfb5504615536b3891ff4ae8a955d8f75bec1d79f58a4518706590c0b53f7883</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2023</creationdate><topic>Animals</topic><topic>Biopsy</topic><topic>Blood plasma</topic><topic>Cardiac muscle</topic><topic>Cardiology</topic><topic>Cardiomyocytes</topic><topic>Cardiomyopathy</topic><topic>Cardiovascular diseases</topic><topic>Congestive heart failure</topic><topic>CpG islands</topic><topic>Deoxyribonucleic acid</topic><topic>Diagnostic systems</topic><topic>Dilated cardiomyopathy</topic><topic>DNA</topic><topic>DNA Methylation</topic><topic>Epigenesis, Genetic</topic><topic>Epigenetics</topic><topic>Epigenomics</topic><topic>Heart failure</topic><topic>Heart Failure - diagnosis</topic><topic>Heart Failure - genetics</topic><topic>Heart Failure - pathology</topic><topic>Humans</topic><topic>Hypertrophy</topic><topic>Induced Pluripotent Stem Cells</topic><topic>Medicine</topic><topic>Medicine & Public Health</topic><topic>Myocardium</topic><topic>Myocytes</topic><topic>Myocytes, Cardiac - pathology</topic><topic>Neonates</topic><topic>Original Contribution</topic><topic>Phenotyping</topic><topic>Plasma</topic><topic>Pluripotency</topic><topic>Rats</topic><topic>Stem cells</topic><topic>Ventricle</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Oeing, Christian U.</creatorcontrib><creatorcontrib>Pepin, Mark E.</creatorcontrib><creatorcontrib>Saul, Kerstin B.</creatorcontrib><creatorcontrib>Agircan, Ayça Seyhan</creatorcontrib><creatorcontrib>Assenov, Yassen</creatorcontrib><creatorcontrib>Merkel, Tobias S.</creatorcontrib><creatorcontrib>Sedaghat-Hamedani, Farbod</creatorcontrib><creatorcontrib>Weis, Tanja</creatorcontrib><creatorcontrib>Meder, Benjamin</creatorcontrib><creatorcontrib>Guan, Kaomei</creatorcontrib><creatorcontrib>Plass, Christoph</creatorcontrib><creatorcontrib>Weichenhan, Dieter</creatorcontrib><creatorcontrib>Siede, Dominik</creatorcontrib><creatorcontrib>Backs, Johannes</creatorcontrib><collection>Springer Nature OA/Free Journals</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>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>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Basic research in cardiology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Oeing, Christian U.</au><au>Pepin, Mark E.</au><au>Saul, Kerstin B.</au><au>Agircan, Ayça Seyhan</au><au>Assenov, Yassen</au><au>Merkel, Tobias S.</au><au>Sedaghat-Hamedani, Farbod</au><au>Weis, Tanja</au><au>Meder, Benjamin</au><au>Guan, Kaomei</au><au>Plass, Christoph</au><au>Weichenhan, Dieter</au><au>Siede, Dominik</au><au>Backs, Johannes</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Indirect epigenetic testing identifies a diagnostic signature of cardiomyocyte DNA methylation in heart failure</atitle><jtitle>Basic research in cardiology</jtitle><stitle>Basic Res Cardiol</stitle><addtitle>Basic Res Cardiol</addtitle><date>2023-03-20</date><risdate>2023</risdate><volume>118</volume><issue>1</issue><spage>9</spage><epage>9</epage><pages>9-9</pages><artnum>9</artnum><issn>1435-1803</issn><issn>0300-8428</issn><eissn>1435-1803</eissn><abstract>Precision-based molecular phenotyping of heart failure must overcome limited access to cardiac tissue. Although epigenetic alterations have been found to underlie pathological cardiac gene dysregulation, the clinical utility of myocardial epigenomics remains narrow owing to limited clinical access to tissue. Therefore, the current study determined whether patient plasma confers indirect phenotypic, transcriptional, and/or epigenetic alterations to ex vivo cardiomyocytes to mirror the failing human myocardium. Neonatal rat ventricular myocytes (NRVMs) and single-origin human induced pluripotent stem cell-derived cardiomyocytes (
hiPSC-CMs
) and were treated with blood plasma samples from patients with dilated cardiomyopathy (DCM) and donor subjects lacking history of cardiovascular disease. Following plasma treatments, NRVMs and
hiPSC-CMs
underwent significant hypertrophy relative to non-failing controls, as determined via automated high-content screening. Array-based DNA methylation analysis of plasma-treated
hiPSC-CMs
and cardiac biopsies uncovered robust, and conserved, alterations in cardiac DNA methylation, from which 100 sites were validated using an independent cohort. Among the CpG sites identified, hypo-methylation of the
ATG
promoter was identified as a diagnostic marker of HF, wherein cg03800765 methylation (AUC = 0.986,
P
< 0.0001) was found to out-perform circulating NT-proBNP levels in differentiating heart failure. Taken together, these findings support a novel approach of indirect epigenetic testing in human HF.</abstract><cop>Berlin/Heidelberg</cop><pub>Springer Berlin Heidelberg</pub><pmid>36939901</pmid><doi>10.1007/s00395-022-00954-3</doi><tpages>1</tpages><orcidid>https://orcid.org/0000-0002-2322-2699</orcidid><oa>free_for_read</oa></addata></record> |
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| language | eng |
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| source | MEDLINE; SpringerLink Journals |
| subjects | Animals Biopsy Blood plasma Cardiac muscle Cardiology Cardiomyocytes Cardiomyopathy Cardiovascular diseases Congestive heart failure CpG islands Deoxyribonucleic acid Diagnostic systems Dilated cardiomyopathy DNA DNA Methylation Epigenesis, Genetic Epigenetics Epigenomics Heart failure Heart Failure - diagnosis Heart Failure - genetics Heart Failure - pathology Humans Hypertrophy Induced Pluripotent Stem Cells Medicine Medicine & Public Health Myocardium Myocytes Myocytes, Cardiac - pathology Neonates Original Contribution Phenotyping Plasma Pluripotency Rats Stem cells Ventricle |
| title | Indirect epigenetic testing identifies a diagnostic signature of cardiomyocyte DNA methylation in heart failure |
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