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CM), suggesting that HNF4-depleted cells with dysregulated SAA metabolism already experience elevated oxidative stress under normal condition and are nonresponsive to further cellular stress induced by methionine/cystine restriction

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Furthermore, experimental evidence has shown that GDF15 may influence pain modulation by reducing nociceptive neuron excitability through peripheral mechanisms involving Nav1.8 sodium channel suppression and modulation of protein kinase A (PKA) and extracellular signal-regulated kinase (ERK) signaling pathways 26,27,28,29