<HashMap><database>biostudies-literature</database><scores/><additional><omics_type>Unknown</omics_type><volume>11</volume><submitter>Vasquez-Trincado C</submitter><funding>Agencia Nacional de Investigación y Desarrollo</funding><pubmed_abstract>&lt;b>Introduction:&lt;/b> Cardiovascular diseases, especially metabolic-related disorders, are progressively growing worldwide due to high-fat-containing foods, which promote a deleterious response at the cellular level, termed lipotoxicity, or lipotoxic stress. At the cardiac level, saturated fatty acids have been directly associated with cardiomyocyte lipotoxicity through various pathological mechanisms involving mitochondrial dysfunction, oxidative stress, and ceramide production, among others. However, integrative regulators connecting saturated fatty acid-derived lipotoxic stress to mitochondrial and cardiomyocyte dysfunction remain elusive. &lt;b>Methods:&lt;/b> Here, we worked with a cardiomyocyte lipotoxicity model, which uses the saturated fatty acid myristate, which promotes cardiomyocyte h</pubmed_abstract><journal>Frontiers in cell and developmental biology</journal><pagination>1072315</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC10083258</full_dataset_link><repository>biostudies-literature</repository><pubmed_title>Myristate induces mitochondrial fragmentation and cardiomyocyte hypertrophy through mitochondrial E3 ubiquitin ligase MUL1.</pubmed_title><pmcid>PMC10083258</pmcid><pubmed_authors>Vasquez-Trincado C</pubmed_authors><pubmed_authors>Chiong M</pubmed_authors><pubmed_authors>Parra V</pubmed_authors><pubmed_authors>Navarro-Marquez M</pubmed_authors><pubmed_authors>Lavandero S</pubmed_authors><pubmed_authors>Espinosa A</pubmed_authors><pubmed_authors>Westermeier F</pubmed_authors><pubmed_authors>Morales PE</pubmed_authors></additional><is_claimable>false</is_claimable><name>Myristate induces mitochondrial fragmentation and cardiomyocyte hypertrophy through mitochondrial E3 ubiquitin ligase MUL1.</name><description>&lt;b>Introduction:&lt;/b> Cardiovascular diseases, especially metabolic-related disorders, are progressively growing worldwide due to high-fat-containing foods, which promote a deleterious response at the cellular level, termed lipotoxicity, or lipotoxic stress. At the cardiac level, saturated fatty acids have been directly associated with cardiomyocyte lipotoxicity through various pathological mechanisms involving mitochondrial dysfunction, oxidative stress, and ceramide production, among others. However, integrative regulators connecting saturated fatty acid-derived lipotoxic stress to mitochondrial and cardiomyocyte dysfunction remain elusive. &lt;b>Methods:&lt;/b> Here, we worked with a cardiomyocyte lipotoxicity model, which uses the saturated fatty acid myristate, which promotes cardiomyocyte h</description><dates><release>2023-01-01T00:00:00Z</release><publication>2023</publication><modification>2026-07-14T22:25:05.531Z</modification><creation>2025-04-05T21:10:41.351Z</creation></dates><accession>S-EPMC10083258</accession><cross_references><pubmed>37051468</pubmed><doi>10.3389/fcell.2023.1072315</doi></cross_references></HashMap>