A biological marker for diagnosis and treatment of preeclampsia and application thereof

By using diagnostic and therapeutic reagents for FBP2 and leveraging the high expression mechanism of FBP2 in placental tissues in preeclampsia, the problem of unclear etiology of preeclampsia has been solved, enabling early prediction and treatment in clinical practice.

CN119351541BActive Publication Date: 2025-12-09NANJING MATERNITY & CHILD HEALTH CARE HOSPITAL
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Patent Information

Application Number
CN202411511838.7
Authority / Receiving Office
CN · China
Patent Type
Patents(China)
Current Assignee / Owner
Filing Date
2024-10-28
Publication Date
2025-12-09
Estimated Expiration
2044-10-28

AI Technical Summary

Technical Problem

The etiology and pathogenesis of preeclampsia are still unclear, and current technologies lack effective diagnostic and therapeutic targets, which affects the health of pregnant women and perinatal infants.

Method used

The study found that FBP2 is significantly upregulated in placental tissue in preeclampsia. As a transcriptional repressor of HEY1, a classic downstream target gene of NOTCH3, FBP2 binds to and binds to the FBP2 promoter region, inhibiting FBP2 expression and thereby regulating c-MYC and TFAM, affecting the migration and invasion ability of trophoblast cells. This provides FBP2 reagents for diagnosis and treatment.

Benefits of technology

FBP2 can serve as a biological marker for preeclampsia, aiding in early prediction and diagnosis, and providing a theoretical basis for clinical treatment. By inhibiting FBP2 expression, trophoblast function can be improved, reducing the incidence of preeclampsia.

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Abstract

The application discloses a kind of preeclampsia (Preeclampsia, PE) diagnosis and treatment biology marker and its application;The application is from clinical sample, cell and in-depth demonstration of overexpressed FBP2 at the level of body, which causes the mechanism of PE occurrence by inhibiting the invasion of trophoblasts, and the application verifies that the classic gene HEY1 downstream of NOTCH3 can be combined with the promoter region of FBP2 and transcribe to inhibit the expression of FBP2, FBP2 is combined with c-MYC protein and inhibits the transcriptional activity of c-MYC, down-regulates the transcriptional expression of TFAM, causes mitochondrial dysfunction, weakens the migration and invasion ability of trophoblasts, participates in the mechanism of PE occurrence, is a new mechanism clue obtained according to the results of pre-experiment and information analysis, is a new target for in-depth exploration of PE clinical diagnosis and treatment, and the research results can provide theoretical basis for guiding early prediction and intervention of PE in the future.
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