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New inhibitors that target this protease successfully block viral replication, offering a dual therapeutic strategy: they inhibit the viral enzyme and disrupt the host lipid environment essential for the virus (45, 58)

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Upon activation by conditions inducing ER stress, CHAC1 expression is upregulated primarily through the PERK-eIF2-ATF3/4 signaling pathway, independent of other UPR branches like IRE1-XBP1

An overview on HMGB1 inhibitors as potential therapeutic agents in HMGB1-related pathologies

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