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Proposed mechanisms mediated by kallistatin in sepsis-induced inflammation, organ injury and mortality. Kallistatin, via its heparin-binding domain, antagonizes TNF-α- and HMGB1-mediated inflammatory gene expression, and its active site is essential for inducing SOCS3 expression. HMGB1, high mobility group box-1; SOCS3, suppressor of cytokine signaling-3; TNF-α, tumor necrosis factor-α.
