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ER Ca 2+ release, sustained store-operated Ca 2+ entry, and persistent cytosolic Ca 2+ elevation can continue to damage PACs even when mitochondrial Ca 2+ entry through MCU is reduced, because calcium-dependent digestive enzyme activation, PM injury, and failure of ATP-dependent ion pumps remain operative

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In line with the reduced isotope tracing data, the total amount of NADH, a product of the TCA cycle, was reduced in HDV-infected cultures (Fig