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Animal data and clinical studies indicate that prolonged use may lead to biosafety concerns such as hematological toxicity and depletion of essential trace elements [176, 178]

However, the precise mechanisms by which activated GSDMD signals back to enhance oxidative stress and promote HC death are not yet fully understood

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Previous research has suggested that hepatic GJ proteins might facilitate the spread of free radicals, thereby exacerbating the severity of drug-induced liver damage (Patel et al

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