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Explores EP4's role in dendritic cell maturation and glycolysis in unexplained recurrent miscarriage, suggesting therapeutic potential.
) in uRM decidua versus healthy controls. Double immunofluorescence demonstrated lower EP4 expression in mature DCs than immature DCs. In vitro, EP4 inhibition promoted monocyte-derived DC maturation (upregulated CD86/CD80) and pro-inflammatory cytokine secretion (TNF-α, IL-6, IL-12), while EP4 activation suppressed these effects. Seahorse analysis showed EP4 blockade enhanced glycolysis via upregulating HK2/PKM2, whereas EP4 activation maintained oxidative metabolism. Mechanistically, EP4 knockdown in DCs suppressed PI3K-AKT-mTOR signaling. These findings suggest that EP4 may be involved in DC maturation through modulation of glycolytic metabolism and PI3K-AKT-mTOR signaling in uRM, while EP4 agonism preserves DC immaturity and metabolic quiescence, suggesting EP4 as a potential therapeutic target for restoring maternal-fetal immune homeostasis in uRM.
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Peng et al. (2026) studied this question.
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