{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Sorge M"],"funding":["Associazione Italiana per la Ricerca sul Cancro","Progetto di Ricerca Nazionale 2022 PNRR","NIDDK NIH HHS","Progetto di Ricerca di Interesse Nazionale 2015","NHLBI NIH HHS","HHS | NIH | National Heart, Lung, and Blood Institute","Compagnia di San Paolo (CSP)","Compagnia di San Paolo"],"pagination":["2450-2484"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC11473679"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["16(10)"],"pubmed_abstract":["Defining the molecular mechanisms underlying cardiac resilience is crucial to find effective approaches to protect the heart. A physiologic level of ROS is produced in the heart by fatty acid oxidation, but stressful events can boost ROS and cause mitochondrial dysfunction and cardiac functional impairment. Melusin is a muscle specific chaperone required for myocardial compensatory remodeling during stress. Here we report that Melusin localizes in mitochondria where it binds the mitochondrial trifunctional protein, a key enzyme in fatty acid oxidation, and decreases it activity. Studying both mice and human induced pluripotent stem cell-derived cardiomyocytes, we found that Melusin reduces lipid oxidation in the myocardium and limits ROS generation in steady state and during pressure overl"],"journal":["EMBO molecular medicine"],"pubmed_title":["An intrinsic mechanism of metabolic tuning promotes cardiac resilience to stress."],"pmcid":["PMC11473679"],"funding_grant_id":["IG29250","CSTO165798","P30 DK017047","IG21408","R01 HL149734","2015EASE8Z","P20225EMBT"],"pubmed_authors":["Penna C","Sorge M","Raimondi A","Tacchetti C","Riganti C","Bertero A","Nattenberg G","Moiso E","Raffaelli N","Gallo A","Ghigo A","Tarone G","Hirsch E","Sbroggio M","Turco E","Savore G","Zamporlini F","Brancaccio M","Corsetto P","Pagliaro P","Velasco S","Stefania R","Femmino S","Balmas E","Altruda F","Pinton P","Sniadecki NJ","Silengo L","Acquarone D","Morciano G","Rizzo AM"],"additional_accession":[]},"is_claimable":false,"name":"An intrinsic mechanism of metabolic tuning promotes cardiac resilience to stress.","description":"Defining the molecular mechanisms underlying cardiac resilience is crucial to find effective approaches to protect the heart. A physiologic level of ROS is produced in the heart by fatty acid oxidation, but stressful events can boost ROS and cause mitochondrial dysfunction and cardiac functional impairment. Melusin is a muscle specific chaperone required for myocardial compensatory remodeling during stress. Here we report that Melusin localizes in mitochondria where it binds the mitochondrial trifunctional protein, a key enzyme in fatty acid oxidation, and decreases it activity. Studying both mice and human induced pluripotent stem cell-derived cardiomyocytes, we found that Melusin reduces lipid oxidation in the myocardium and limits ROS generation in steady state and during pressure overl","dates":{"release":"2024-01-01T00:00:00Z","publication":"2024 Oct","modification":"2026-07-15T05:33:40.51Z","creation":"2025-04-04T08:21:24.087Z"},"accession":"S-EPMC11473679","cross_references":{"pubmed":["39271959"],"doi":["10.1038/s44321-024-00132-z"]}}