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It is produced in every cell and plays a central role in protecting cells from oxidative stress and supporting detoxification processes

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Substantiating this mechanism, murine studies with macrophage-specific deletion of myeloid differentiation primary response 88 (MyD88) demonstrated that inhibition of TLR/NF-B-mediated macrophage inflammation significantly attenuates hepatic lipid accumulation and injury in NAFLD models [87]

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