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10.1016/j.cell.2018.09.048 Cell 32 LiG.LiX.DongJ.HanY
It significantly elevates the pro-atherogenic metabolite TMAO by upregulating hepatic FMO3, independent of changes in gut TMA-lyase activity (Wang et al., 2024)
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Mitophagy constitutes a critical adaptive survival mechanism for tumor cells under therapeutic pressure by eliminating treatment-induced damaged mitochondria, limiting reactive oxygen species accumulation, and maintaining mitochondrial homeostasis, thereby providing a buffering capacity for the development of resistance
In contrast, although BFA treatment induced SLC7A11 to be stuck in the ER, only ~15% of VRK-KO cells returned SLC7A11 to the Golgi 4 h after BFA removal
Michalikov D, Hrn T, Canov NK, Slana O (2020a) Targeting Keap1/Nrf2/ARE signaling pathway in multiple sclerosis
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