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[] This study identified H3K9me3-mediated repression of mitochondrial genes as a key epigenetic mechanism in HF progression, positioning H3K9 methyltransferase inhibitors as promising therapeutic agents targeting metabolic dysfunction in chronic HF

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OSBPL2 is required for the binding of COPB1 to ATGL and the regulation of lipid droplet lipolysis

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meet their B-12 needs, uncertainties persist