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Thus, miR-34a acts as a disease-promoting factor in this process: its high expression accelerates lipid accumulation and exacerbates MAFLD development, whereas exercise-induced ADAR2 improves MAFLD by inhibiting miR-34a

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This gap forces clinicians to rely on clinical assessment and imaging, both of which have substantial limitations, or to proceed directly to surgical diagnosis for definitive confirmation

Incorporating analogous mitochondria directed GSH-sensing reporters into nanoplatforms would allow simultaneous readout and modulation of intramitochondrial redox status, enabling closed-loop theranostic schemes i.e