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Identifies prokineticin 2's role in impairing trophoblast function in preeclampsia, suggesting a new target for treatment.
This study identifies PK2 as a key pathogenic factor in PE that impairs trophoblast function. The findings suggest that its mechanism may involve the induction of AP-1 components. Our work provides the first evidence positioning the PK2/PKR2 axis as a novel contributor to PE pathogenesis and a potential therapeutic target.
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Li et al. (2026) studied this question.
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