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This leads to the release and cytoplasmic translocation of p53, which can subsequently activate transcription-independent pro-apoptotic signaling (Clara et al., 2024
Consequently, TMAO also participates in the formation of NOCs, leading to DNA damage and epigenetic changes, indicating a potential role of DNA damage in TMAOs carcinogenic effects (Oellgaard et al., 2017)
2025;11:e41114
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