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Low zinc levels heighten endothelial cell vulnerability to LPS-induced apoptosis, whereas higher intracellular zinc supports defenses against apoptosis, possibly via nitric oxide pathways [473]

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The result is a systems-level approach to digestive health, with butyrate at the center as the key metabolite.

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A hallmark of cuproptosis is the aggregation of lipoylated dihydrolipoamide S-acetyltransferase (DLAT), implicated in Wilson disease [54]

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