Experimental analysis shows Gzma disrupts the intestinal barrier in sepsis, indicating potential therapeutic targets.
Gzma induces the dephosphorylation of Ser886 on GEF-H1, activating the RhoA/ROCK pathway and disrupting the intestinal epithelial barrier. Knocking out GEF-H1 can alleviate intestinal damage, protect multiple organs, and increase the survival rate of septic mice. Epothilone A inhibits the activation of GEF-H1, thereby restoring the barrier function and reducing the mortality rate of sepsis.
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Lin et al. (2026) studied this question.
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