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ROS mediates inflammation, mitochondrial damage, and cell death, ultimately promoting liver damage. KCs recognize HMGB1, promote the inflammatory response through the TRL4-MyD88-NF-κB pathway. At the same time, TNF-α activated by ROS, phosphorylating JNK and further producing ROS. Activated TNF-α also form complexes that activate caspase 8, leading to mitochondrial permeability transition (MTP) and finally apoptosis.
