Ontology highlight
ABSTRACT: Alterations in myocardial energy substrate metabolism following myocardial infarction (MI) results in structural and functional abnormalities of the heart. The fatty acid translocase CD36 (CD36), acrucial membrane protein, plays a pivotal role in regulating fatty acid (FA) uptake and lipid homeostasis. Here, we employed a comprehensive multi-omics analysis using a mouse MI model, integrating molecular biology, histological, transcriptomic and proteomic analyses. Our findings unveiled dysregulation in lipid metabolism, mitochondrial oxidative phosphorylation and related genes.
INSTRUMENT(S): Liquid Chromatography MS - negative - reverse phase, Liquid Chromatography MS - positive - reverse phase
PROVIDER: MTBLS12600 | MetaboLights | 2025-06-15
REPOSITORIES: MetaboLights
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