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The gut microbiota metabolite glycochenodeoxycholate activates TFR-ACSL4-mediated ferroptosis to promote the development of environmental toxin-linked MAFLD
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Under normal physiological conditions, the HGF/c-MET signaling pathway is tightly regulated by negative feedback mechanisms
Compared to M-CuP, D-CuP exhibited significantly higher proliferative activity at lower concentrations, which was more conducive to wound healing
Facilitating AKT clearance via manipulation of Hsp70 activity and levels
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