<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Sama IE</submitter><funding>National Institute for Health Research (NIHR)</funding><pagination>821-833</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC7319432</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>22(5)</volume><pubmed_abstract>&lt;h4>Aims&lt;/h4>Heart failure (HF) is frequently caused by an ischaemic event (e.g. myocardial infarction) but might also be caused by a primary disease of the myocardium (cardiomyopathy). In order to identify targeted therapies specific for either ischaemic or non-ischaemic HF, it is important to better understand differences in underlying molecular mechanisms.&lt;h4>Methods and results&lt;/h4>We performed a biological physical protein-protein interaction network analysis to identify pathophysiological pathways distinguishing ischaemic from non-ischaemic HF. First, differentially expressed plasma protein biomarkers were identified in 1160 patients enrolled in the BIOSTAT-CHF study, 715 of whom had ischaemic HF and 445 had non-ischaemic HF. Second, we constructed an enriched physical protein-protei</pubmed_abstract><journal>European journal of heart failure</journal><pubmed_title>A network analysis to identify pathophysiological pathways distinguishing ischaemic from non-ischaemic heart failure.</pubmed_title><pmcid>PMC7319432</pmcid><funding_grant_id>NF-SI-0611-10170</funding_grant_id><pubmed_authors>Nauta JF</pubmed_authors><pubmed_authors>Ter Maaten JM</pubmed_authors><pubmed_authors>Zannad F</pubmed_authors><pubmed_authors>Cleland JGF</pubmed_authors><pubmed_authors>Metra M</pubmed_authors><pubmed_authors>van der Meer P</pubmed_authors><pubmed_authors>Sama IE</pubmed_authors><pubmed_authors>Hillege HL</pubmed_authors><pubmed_authors>Lang CC</pubmed_authors><pubmed_authors>Samani NJ</pubmed_authors><pubmed_authors>Voors AA</pubmed_authors><pubmed_authors>Romaine SPR</pubmed_authors><pubmed_authors>Dickstein K</pubmed_authors><pubmed_authors>Anker SD</pubmed_authors><pubmed_authors>Lam CSP</pubmed_authors><pubmed_authors>Woolley RJ</pubmed_authors><pubmed_authors>Tromp J</pubmed_authors><pubmed_authors>Ng LL</pubmed_authors><pubmed_authors>van Veldhuisen DJ</pubmed_authors></additional><is_claimable>false</is_claimable><name>A network analysis to identify pathophysiological pathways distinguishing ischaemic from non-ischaemic heart failure.</name><description>&lt;h4>Aims&lt;/h4>Heart failure (HF) is frequently caused by an ischaemic event (e.g. myocardial infarction) but might also be caused by a primary disease of the myocardium (cardiomyopathy). In order to identify targeted therapies specific for either ischaemic or non-ischaemic HF, it is important to better understand differences in underlying molecular mechanisms.&lt;h4>Methods and results&lt;/h4>We performed a biological physical protein-protein interaction network analysis to identify pathophysiological pathways distinguishing ischaemic from non-ischaemic HF. First, differentially expressed plasma protein biomarkers were identified in 1160 patients enrolled in the BIOSTAT-CHF study, 715 of whom had ischaemic HF and 445 had non-ischaemic HF. Second, we constructed an enriched physical protein-protei</description><dates><release>2020-01-01T00:00:00Z</release><publication>2020 May</publication><modification>2025-04-22T06:39:56.072Z</modification><creation>2020-07-03T07:08:32Z</creation></dates><accession>S-EPMC7319432</accession><cross_references><pubmed>32243695</pubmed><doi>10.1002/ejhf.1811</doi></cross_references></HashMap>