HMGB1 Modulates Angiogenic Imbalance and Cardiovascular Complications in Preeclampsia through Decorin and VEGF Regulation.

BACKGROUND

Preeclampsia (PE) is a serious multisystem disorder that ranks among the leading causes of maternal and neonatal morbidity and mortality. The condition is characterized by an angiogenic imbalance, which has adverse effects on fetal development and contributes to an increased risk of cardiovascular disease in the long term. This study aims to explore the connection between sterile inflammation mediated by HMGB1 and angiogenic imbalance in PE by examining key markers such as HMGB1, VEGF, Decorin, and TGF-β.

METHODS

In an animal model of PE, we measured the levels of HMGB1, VEGF, Decorin, and TGF-β in plasma, placenta, and heart tissues using ELISA. Additionally, Decorin levels were assessed through immunofluorescence in trophoblasts.

RESULTS

We found that levels of Decorin and TGF-β were significantly elevated in the plasma, placenta, and heart tissues of PE animals compared to non-pregnant and pregnant controls, whereas VEGF levels were reduced. Treatment with Glycyrrhizic acid (GA) restored the expression levels of these markers to more normalized values in the PE groups.

CONCLUSIONS

Our findings indicate that HMGB1 plays a critical role in preeclampsia by mediating the upregulation of anti-angiogenic factors like Decorin and the downregulation of angiogenic factors like VEGF. This study highlights a significant correlation between HMGB1 and Decorin in driving the angiogenic imbalance that contributes to the pathophysiology of PE.