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In the early stages of atherosclerosis, macrophages bind to lipopolysaccharides to promote cholesterol accumulation, lipid accumulation in plaques, and foam cell formation, which is a hallmark of atherosclerotic lesions

19 Following further translocation to the mitochondria, activated phosphorylated JNK initiates a cascade in which JNK binds to the outer mitochondrial membrane scaffold protein Sab, inhibiting electron transport and thereby increasing the generation of ROS and peroxynitrite

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For example, flubendazole combined with 5-FU can induce CRPC death by promoting ferroptosis [28]

It is a growth hormone secretagogue (GHS) that activates the ghrelin receptor (GHS-R1a) not the GHRH receptor