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The reduction in hepatic fat in HIV-associated fatty liver disease, alongside the primary visceral-fat effect, has been characterized in randomized trials, and the mechanistic follow-up identified reductions in fibro-inflammatory mediators (VEGFA, TGF-1, CSF1) that track with improvements in liver-injury scores

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This review synthesizes mechanistic insights from redox biology and immunometabolism to clinical trial data, proposing a framework for optimizing VC-based combination therapies while addressing critical gaps in biomarker development and dose scheduling

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