Experimental findings demonstrate IL-36G's role in lung injury during sepsis, indicating possible therapeutic targets.
IL-36G promoted pyroptosis and NLRP3 inflammasome activation via NF-κB signaling pathway, contributing to sepsis-induced lung injury. Knockdown of IL-36G mitigated inflammation and tissue damage, indicating the therapeutic potential of IL-36G in sepsis.
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Yan et al. (2026) studied this question.
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