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For instance, TMAO triggers NLRP3 inflammasome formation and activates NF-B signaling, Caspase-1, the PERK/Akt/mTOR pathway, and IL-1, leading to increased renal fibrosis ( in vitro study found that TMAO down-regulates Gadd45a expression by mediating the nuclear translocation of Y-box binding protein-1, thus inhibiting cell cycle progression ( In summary, TMAO contributes to CKD progression, indicating that targeting TMAO could be a promising treatment strategy

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These results confirm that PCa treated by ALCAR are less pro-angiogenic in vitro by inducing less HUVE capillary-like morphogenesis