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disruption of this axis promotes energetic depletion, oxidative stress, inflammasome activation, and progression of cellular injury ( 3.9 Summary Taken together, the available experimental evidence supports a hierarchical model of AP pathogenesis centered on the mitochondrial hub ( Figure 3 ), in which early pathogenic triggers, including toxic calcium signals, bile acid exposure, alcohol metabolites, hyperstimulation, and lipotoxic stress, initiate progressive remodeling of mitochondrial contact sites with the ER, lysosomes, the cytoskeleton, and other organelles

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