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The above pathological changes were significantly alleviated by Rd in a dose-dependent manner (Fig

4-HNE represents a highly reactive lipid peroxidation byproduct that induces cellular damage by interacting with proteins, DNA, and other cellular components through iron- and oxygen-mediated chain-breaking reactions ( The transient receptor potential channel TRPM4 has been shown to promote ox-LDL-induced dysfunction in HCAECs through ferroptosis mechanisms ( Additionally, reduced sterol regulatory element-binding protein 1 (SREBP-1) expressiona key transcription factor in lipid and cholesterol metabolismis associated with stable CAD development

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