<HashMap><database>biostudies-literature</database><scores/><additional><omics_type>Unknown</omics_type><volume>9</volume><submitter>Skeffington KL</submitter><funding>British Heart Foundation</funding><pubmed_abstract>&lt;h4>Background&lt;/h4>Mature cardiomyocytes are unable to proliferate, preventing the injured adult heart from repairing itself. Studies in rodents have suggested that the extracellular matrix protein agrin promotes cardiomyocyte proliferation in the developing heart and that agrin expression is downregulated shortly after birth, resulting in the cessation of proliferation. Agrin based therapies have proven successful at inducing repair in animal models of cardiac injury, however whether similar pathways exist in the human heart is unknown.&lt;h4>Methods&lt;/h4>Right ventricular (RV) biopsies were collected from 40 patients undergoing surgery for congenital heart disease and the expression of agrin and associated proteins was investigated.&lt;h4>Results&lt;/h4>Agrin transcripts were found in all samples </pubmed_abstract><journal>Frontiers in cardiovascular medicine</journal><pagination>813904</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC8959542</full_dataset_link><repository>biostudies-literature</repository><pubmed_title>Determination of Agrin and Related Proteins Levels as a Function of Age in Human Hearts.</pubmed_title><pmcid>PMC8959542</pmcid><pubmed_authors>Jones FP</pubmed_authors><pubmed_authors>Bigotti MG</pubmed_authors><pubmed_authors>Brancaccio A</pubmed_authors><pubmed_authors>Skeffington KL</pubmed_authors><pubmed_authors>Caputo M</pubmed_authors><pubmed_authors>Suleiman MS</pubmed_authors></additional><is_claimable>false</is_claimable><name>Determination of Agrin and Related Proteins Levels as a Function of Age in Human Hearts.</name><description>&lt;h4>Background&lt;/h4>Mature cardiomyocytes are unable to proliferate, preventing the injured adult heart from repairing itself. Studies in rodents have suggested that the extracellular matrix protein agrin promotes cardiomyocyte proliferation in the developing heart and that agrin expression is downregulated shortly after birth, resulting in the cessation of proliferation. Agrin based therapies have proven successful at inducing repair in animal models of cardiac injury, however whether similar pathways exist in the human heart is unknown.&lt;h4>Methods&lt;/h4>Right ventricular (RV) biopsies were collected from 40 patients undergoing surgery for congenital heart disease and the expression of agrin and associated proteins was investigated.&lt;h4>Results&lt;/h4>Agrin transcripts were found in all samples </description><dates><release>2022-01-01T00:00:00Z</release><publication>2022</publication><modification>2025-04-19T00:40:57.113Z</modification><creation>2025-04-07T11:44:59.989Z</creation></dates><accession>S-EPMC8959542</accession><cross_references><pubmed>35355976</pubmed><doi>10.3389/fcvm.2022.813904</doi></cross_references></HashMap>