<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Forini F</submitter><funding>Tuscany Region Research Grant</funding><pagination>26687-705</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC4661832</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>16(11)</volume><pubmed_abstract>Mitochondria are major determinants of cell fate in ischemia/reperfusion injury (IR) and common effectors of cardio-protective strategies in cardiac ischemic disease. Thyroid hormone homeostasis critically affects mitochondrial function and energy production. Since a low T3 state (LT3S) is frequently observed in the post infarction setting, the study was aimed to investigate the relationship between 72 h post IR T3 levels and both the cardiac function and the mitochondrial proteome in a rat model of IR. The low T3 group exhibits the most compromised cardiac performance along with the worst mitochondrial activity. Accordingly, our results show a different remodeling of the mitochondrial proteome in the presence or absence of a LT3S, with alterations in groups of proteins that play a key rol</pubmed_abstract><journal>International journal of molecular sciences</journal><pubmed_title>Low T3 State Is Correlated with Cardiac Mitochondrial Impairments after Ischemia Reperfusion Injury: Evidence from a Proteomic Approach.</pubmed_title><pmcid>PMC4661832</pmcid><funding_grant_id>DGR 1157/2011</funding_grant_id><pubmed_authors>Nicolini G</pubmed_authors><pubmed_authors>Iervasi G</pubmed_authors><pubmed_authors>Forini F</pubmed_authors><pubmed_authors>Citti L</pubmed_authors><pubmed_authors>Cecchettini A</pubmed_authors><pubmed_authors>Rocchiccioli S</pubmed_authors><pubmed_authors>Ucciferri N</pubmed_authors><pubmed_authors>Kusmic C</pubmed_authors></additional><is_claimable>false</is_claimable><name>Low T3 State Is Correlated with Cardiac Mitochondrial Impairments after Ischemia Reperfusion Injury: Evidence from a Proteomic Approach.</name><description>Mitochondria are major determinants of cell fate in ischemia/reperfusion injury (IR) and common effectors of cardio-protective strategies in cardiac ischemic disease. Thyroid hormone homeostasis critically affects mitochondrial function and energy production. Since a low T3 state (LT3S) is frequently observed in the post infarction setting, the study was aimed to investigate the relationship between 72 h post IR T3 levels and both the cardiac function and the mitochondrial proteome in a rat model of IR. The low T3 group exhibits the most compromised cardiac performance along with the worst mitochondrial activity. Accordingly, our results show a different remodeling of the mitochondrial proteome in the presence or absence of a LT3S, with alterations in groups of proteins that play a key rol</description><dates><release>2015-01-01T00:00:00Z</release><publication>2015 Nov</publication><modification>2026-05-05T07:33:57.463Z</modification><creation>2025-05-18T11:59:50.293Z</creation></dates><accession>S-EPMC4661832</accession><cross_references><pubmed>26561807</pubmed><doi>10.3390/ijms161125973</doi></cross_references></HashMap>