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Recently, ferroptosis has been considered a type of autophagy-dependent cell death due to the selective autophagic degradation of anti-ferroptosis proteins (e.g., ferritin [145,146], BMAL1/ARNTL [basic helix-loop-helix ARNT like 1] [147], SLC40A1/ferroportin-1 [39], or GPX4 [71] as well as organelles [e.g., lipid droplets] [148])

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It activates both GLP-1 and glucagon receptors, with the glucagon component being particularly relevant for hepatic fat metabolism -- a key differentiator that has driven its MASH development program

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