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The mechanisms responsible for acitretin-induced hepatotoxicity involve mitochondrial dysfunction, particularly within hepatocytes

Population-based studies consistently demonstrate that individuals with CVDs face a significantly elevated risk of developing cognitive impairment, including dementia [1, 2]

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Changes to the microbial phyla and genera observed in the 5A-1MQ-treated group switched from WD to LD could have been driven by additive, synergistic, or independent mechanisms relative to those induced by diet switch alone, which could not be determined with the current study design that lacked a group treated with 5A-1MQ and maintained on WD