• Established a novel ALD model using hiPSC-derived liver organoids that recapitulate key pathological features of clinical ALD, including mitochondrial damage, elevated ROS, steatosis, and necrosis.
• The organoid model provides a physiologically relevant 3D platform for drug screening, overcoming limitations of 2D cultures and animal models.
• The differentiation protocol integrates specific cytokines and small molecules to guide hiPSCs into functional liver organoids, offering a reproducible and scalable approach.
• This model holds significant potential for advancing ALD research and developing targeted therapies, bridging the gap between in vitro and in vivo studies.
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