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The results, together with the ability of ascites to protect against ferroptosis triggered by genetic means ( GPX4 knockout in Supplementary Fig

However, under pro-inflammatory conditions, some of the major NAD + consumers, such as PARPs, become highly activated, tilting the scales of NAD + homeostasis toward excessive consumption, quickly depleting intracellular NAD + stores, and leading to mitochondrial dysfunction and impaired energy metabolism (16, 17, 18, 20, 21, 22)

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