ArticleFrontiers in pharmacology2026
Integrated multi-omics reveals acylcarnitine accumulation as an early driver of doxorubicin-induced cardiotoxicity targeted by chlorogenic acid.
Article in Frontiers in pharmacology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Introduction: Doxorubicin (DOX)-induced cardiotoxicity (DIC) is a major clinical challenge, with early metabolic reprogramming acting as a potential pathogenic driver. This study investigates the early lipid metabolic disturbances in DIC and evaluates the cardioprotective potential of the natural metabolic modulator, chlorogenic acid (CGA). Methods: Transcriptomic analysis was utilized to identify initial metabolic alterations. Lipidomics and spatial metabolomics were performed to map lipid distributions in DOX-treated H9c2 cardiomyocytes and C57BL/6J mouse hearts. The therapeutic mechanisms of CGA were assessed Results: Transcriptomics and lipidomics revealed that DOX significantly suppresses the PPAR signaling pathway and fatty acid oxidation (FAO), resulting in the accumulation of ceramides and long-chain acylcarnitines. Spatial metabolomics confirmed Discussion: Impaired FAO and the subsequent accumulation of toxic acylcarnitines serve as early drivers of DOX-induced metabolic dysfunction. Targeting this lipid metabolic dysregulation with CGA represents a promising therapeutic strategy for mitigating anthracycline-induced cardiotoxicity.
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