<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Liu D</submitter><funding>NHLBI NIH HHS</funding><funding>NIGMS NIH HHS</funding><pagination>810-825</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC10746262</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>133(10)</volume><pubmed_abstract>&lt;h4>Background&lt;/h4>Dilated cardiomyopathy (DCM) is a major cause of heart failure and carries a high mortality rate. Myocardial recovery in DCM-related heart failure patients is highly variable, with some patients having little or no response to standard drug therapy. A genome-wide association study may agnostically identify biomarkers and provide novel insight into the biology of myocardial recovery in DCM.&lt;h4>Methods&lt;/h4>A genome-wide association study for change in left ventricular ejection fraction was performed in 686 White subjects with recent-onset DCM who received standard pharmacotherapy. Genome-wide association study signals were subsequently functionally validated and studied in relevant cellular models to understand molecular mechanisms that may have contributed to the change i</pubmed_abstract><journal>Circulation research</journal><pubmed_title>Myocardial Recovery in Recent Onset Dilated Cardiomyopathy: Role of &lt;i>CDCP1&lt;/i> and Cardiac Fibrosis.</pubmed_title><pmcid>PMC10746262</pmcid><funding_grant_id>R01 HL075038</funding_grant_id><funding_grant_id>T32 GM008685</funding_grant_id><funding_grant_id>R01 HL116906</funding_grant_id><funding_grant_id>R01 HL069071</funding_grant_id><funding_grant_id>R01 HL164634</funding_grant_id><pubmed_authors>McNamara DM</pubmed_authors><pubmed_authors>Jenkins GD</pubmed_authors><pubmed_authors>Skime MK</pubmed_authors><pubmed_authors>Barlera S</pubmed_authors><pubmed_authors>Starling RC</pubmed_authors><pubmed_authors>Sahni J</pubmed_authors><pubmed_authors>Gao H</pubmed_authors><pubmed_authors>Nguyen TTL</pubmed_authors><pubmed_authors>Cooper LT</pubmed_authors><pubmed_authors>Wang M</pubmed_authors><pubmed_authors>Mestroni L</pubmed_authors><pubmed_authors>Pinet F</pubmed_authors><pubmed_authors>de Groote P</pubmed_authors><pubmed_authors>Weinshilboum RM</pubmed_authors><pubmed_authors>Murthy V</pubmed_authors><pubmed_authors>Krejci J</pubmed_authors><pubmed_authors>Pereira NL</pubmed_authors><pubmed_authors>Tschumperlin DJ</pubmed_authors><pubmed_authors>Chaloupka A</pubmed_authors><pubmed_authors>Vyas H</pubmed_authors><pubmed_authors>Sinagra G</pubmed_authors><pubmed_authors>Philips TJ</pubmed_authors><pubmed_authors>Batzler A</pubmed_authors><pubmed_authors>Miller JD</pubmed_authors><pubmed_authors>Merlo M</pubmed_authors><pubmed_authors>Liu D</pubmed_authors><pubmed_authors>Pileggi S</pubmed_authors></additional><is_claimable>false</is_claimable><name>Myocardial Recovery in Recent Onset Dilated Cardiomyopathy: Role of &lt;i>CDCP1&lt;/i> and Cardiac Fibrosis.</name><description>&lt;h4>Background&lt;/h4>Dilated cardiomyopathy (DCM) is a major cause of heart failure and carries a high mortality rate. Myocardial recovery in DCM-related heart failure patients is highly variable, with some patients having little or no response to standard drug therapy. A genome-wide association study may agnostically identify biomarkers and provide novel insight into the biology of myocardial recovery in DCM.&lt;h4>Methods&lt;/h4>A genome-wide association study for change in left ventricular ejection fraction was performed in 686 White subjects with recent-onset DCM who received standard pharmacotherapy. Genome-wide association study signals were subsequently functionally validated and studied in relevant cellular models to understand molecular mechanisms that may have contributed to the change i</description><dates><release>2023-01-01T00:00:00Z</release><publication>2023 Oct</publication><modification>2026-06-01T19:43:44.303Z</modification><creation>2025-04-19T17:28:00.795Z</creation></dates><accession>S-EPMC10746262</accession><cross_references><pubmed>37800334</pubmed><doi>10.1161/CIRCRESAHA.123.323200</doi><doi>10.1161/circresaha.123.323200</doi></cross_references></HashMap>