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Regulation of hepatic energy metabolism by the nuclear receptor PXR

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This system uses pathological signals as input and triggers preset functional outputs (e.g., drug release, mechanical enhancement, ECM regeneration, and immune regulation) through specific response mechanisms such as chemical bond breaking/recombination, physical state changes, and biomolecule activation, ultimately enabling accurate intervention in the IVDD process ( 2.3.1 Chemical bond programming: Dynamic covalent/non-covalent bond response Chemical bond programming represents a leading strategy for enabling smart hydrogels to respond to pathological microenvironments (Wang et al., 2024b

PRMT2 (protein arginine methyltransferase 2) promotes the arginine methylation of -catenin, leading to the degradation of -catenin protein and subsequently inhibiting GPX4 transcription