<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Hunter B</submitter><funding>National Heart Foundation of Australia (Heart Foundation)</funding><funding>Federal Government | DHAC | National Health and Medical Research Council</funding><funding>National Heart Foundation of Australia</funding><funding>R.T. Hall Trust</funding><funding>NIDDK NIH HHS</funding><funding>R.T. Hall Trust (Estate of Late R.T. Hall)</funding><funding>Federal Government | DHAC | National Health and Medical Research Council (NHMRC)</funding><funding>NIH HHS</funding><pagination>2483-2524</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC12423312</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>17(9)</volume><pubmed_abstract>Ischaemic cardiomyopathy is the most common cause of heart failure and often coexists with diabetes mellitus, which worsens patient symptom burden and outcomes. Yet, their combined effects are seldom investigated and are poorly understood. To uncover the influencing molecular signature defining ischaemic cardiomyopathy with diabetes, we performed multi-omic analyses of ischaemic and non-ischaemic cardiomyopathy with and without diabetes against healthy age-matched donors. Tissue was sourced from pre-mortem human left ventricular myocardium. Fatty acid transport and oxidation proteins were most downregulated in ischaemic cardiomyopathy with diabetes relative to donors. However, the downregulation of acylcarnitines, perilipin, and ketone body, amino acid, and glucose metabolising proteins in</pubmed_abstract><journal>EMBO molecular medicine</journal><pubmed_title>Left ventricular myocardial molecular profile of human diabetic ischaemic cardiomyopathy.</pubmed_title><pmcid>PMC12423312</pmcid><funding_grant_id>105595</funding_grant_id><funding_grant_id>2024161</funding_grant_id><funding_grant_id>OT2 OD030544</funding_grant_id><funding_grant_id>U2C DK119886</funding_grant_id><funding_grant_id>RQ112</funding_grant_id><funding_grant_id>104853</funding_grant_id><funding_grant_id>G212785</funding_grant_id><pubmed_authors>Khor J</pubmed_authors><pubmed_authors>Rajagopal V</pubmed_authors><pubmed_authors>Dutta S</pubmed_authors><pubmed_authors>Koay YC</pubmed_authors><pubmed_authors>McEwen H</pubmed_authors><pubmed_authors>O'Sullivan JF</pubmed_authors><pubmed_authors>Yang JYH</pubmed_authors><pubmed_authors>Malecki C</pubmed_authors><pubmed_authors>Guglielmi G</pubmed_authors><pubmed_authors>Larance M</pubmed_authors><pubmed_authors>Zhang Y</pubmed_authors><pubmed_authors>Walker A</pubmed_authors><pubmed_authors>Don A</pubmed_authors><pubmed_authors>Lal S</pubmed_authors><pubmed_authors>Hunter B</pubmed_authors><pubmed_authors>Harney D</pubmed_authors><pubmed_authors>Hume RD</pubmed_authors><pubmed_authors>Pan M</pubmed_authors></additional><is_claimable>false</is_claimable><name>Left ventricular myocardial molecular profile of human diabetic ischaemic cardiomyopathy.</name><description>Ischaemic cardiomyopathy is the most common cause of heart failure and often coexists with diabetes mellitus, which worsens patient symptom burden and outcomes. Yet, their combined effects are seldom investigated and are poorly understood. To uncover the influencing molecular signature defining ischaemic cardiomyopathy with diabetes, we performed multi-omic analyses of ischaemic and non-ischaemic cardiomyopathy with and without diabetes against healthy age-matched donors. Tissue was sourced from pre-mortem human left ventricular myocardium. Fatty acid transport and oxidation proteins were most downregulated in ischaemic cardiomyopathy with diabetes relative to donors. However, the downregulation of acylcarnitines, perilipin, and ketone body, amino acid, and glucose metabolising proteins in</description><dates><release>2025-01-01T00:00:00Z</release><publication>2025 Sep</publication><modification>2026-06-01T23:28:10.462Z</modification><creation>2026-05-23T03:08:04.258Z</creation></dates><accession>S-EPMC12423312</accession><cross_references><pubmed>40759793</pubmed><doi>10.1038/s44321-025-00281-9</doi></cross_references></HashMap>