HMGB۱ Modulates Angiogenic Imbalance and Cardiovascular Complications in Preeclampsia through Decorin and VEGF Regulation

سال انتشار: 1403
نوع سند: مقاله ژورنالی
زبان: انگلیسی
مشاهده: 38

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شناسه ملی سند علمی:

JR_RBMB-13-3_010

تاریخ نمایه سازی: 7 اردیبهشت 1404

چکیده مقاله:

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 HMGB۱ and angiogenic imbalance in PE by examining key markers such as HMGB۱, VEGF, Decorin, and TGF-β. Methods: In an animal model of PE, we measured the levels of HMGB۱, 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. Conclusion: Our findings indicate that HMGB۱ 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 HMGB۱ and Decorin in driving the angiogenic imbalance that contributes to the pathophysiology of PE.

کلیدواژه ها:

Angiogenesis Inhibitors ، Cardiovascular Diseases ، Decorin ، Transforming Growth Factor beta ، High Mobility Group Box ۱ Protein ، Preeclampsia.

نویسندگان

Huma Quasimi

Department of Physiology, Hamdard Institute of Medical Sciences and Research, Jamia Hamdard, New Delhi-۱۱۰۰۶۲; Huma.qasimi@gmail.com.

Sheema Wazib

Department of Physiology, Hamdard Institute of Medical Sciences and Research, Jamia Hamdard, New Delhi-۱۱۰۰۶۲; Huma.qasimi@gmail.com.

Gausal Azam Khan

Department of Clinical Nutrition, College of Applied Medical Sciences, King Faisal University, Alhasa, KSA.

Md Iqbal Alam*

Department of Physiology, Hamdard Institute of Medical Sciences and Research, Jamia Hamdard, New Delhi-۱۱۰۰۶۲; Huma.qasimi@gmail.com.

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