ArticleClinical and translational medicine2026
Recipient-derived macrophages mediate acute cardiac allograft rejection via GSDMD-induced pyroptosis mechanism.
Article in Clinical and translational medicine, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
objectiveTo determine whether macrophage gasdermin D (GSDMD)-dependent pyroptosis drives acute cardiac allograft rejection and whether targeting GSDMD improves graft survival.
methodsGSDMD activation was assessed by immunoblotting. Graft survival wasanalysed in global and macrophage-specific GSDMD-deficient recipients. Single-cell RNA-seq identified GSDMD-expressing populations, while immune infiltration and cytokines were measured by flow cytometry and immunohistochemistry; IL1R1 knockout and cytokine challenge were used for validation.
resultsGSDMD deficiency markedly prolonged graft survival. Single-cell profiling showed increased GSDMD expression and pyroptosis primarily in recipient-derived M1 macrophages during acute rejection. Macrophage-specific GSDMD deficiency reduced CD8
conclusionRecipient M1 macrophages promote acute rejection via TNFα/IL6-driven NF-κB/STAT3 activation of GSDMD-mediated pyroptosis. Targeting GSDMD represents a promising strategy to enhance cardiac allograft survival.
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