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In addition, the accumulation of cholesterol in KCs and HSCs accounts for stimulated inflammation and fibrosis, characteristic of the advanced stages of MASLD [87, 121, 122, 133]

IP3 binds to its receptor, IP3R1, resulting in a low concentration of calcium releasing into the ER, and this action induces Duox1, an isoform of NOX, to produce intracellular hydrogen peroxide (35)