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Ullah I, Subbarao RB, Rho GJ

In nonalcoholic fatty liver disease, endogenous denatured DNA, cholesterol, and HMGB1 derived from apoptotic and necrotic host cells, together with mtDNA, formylated peptides, and ATP released due to mitochondrial dysfunction, induce inflammation by activating the cGAS/STING pathway and NLRP3 inflammasomes [267]

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It can be computationally challenging to utilize the strategies pioneered by Yemshanov et al

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