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Both Trim29 and NEDD4L enhanced substrate ubiquitination degradation triggered the NF-B signaling pathway and resulted in podocyte pyroptosis and inflammation, respectively

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Mechanistically distinct from other forms of cell death, cuproptosis is characterized by the direct binding of copper to lipoylated enzymes in the mitochondrial tricarboxylic acid (TCA) cycle, leading to proteotoxic stress and subsequent cell death, independent of classical apoptotic signaling [3]