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Updated: Feb 5, 2026

Author Spotlight: Investigating the Mechanisms and Inducing Models of Polycystic Ovary Syndrome
Published on: July 5, 2024
Serum HMGB1 levels and its association with endothelial dysfunction in patients with polycystic ovary syndrome
Hao-Hua Wang1, Min Lin, Guang-da Xiang
1Department of Endocrinology, Tungwah Hospital of Sun Yat-Sen University, Dongguan, China. hello_vanwang@sohu.com.
Insights
High-mobility group box 1 (HMGB1) is elevated in polycystic ovary syndrome (PCOS) and linked to endothelial dysfunction. Metformin treatment reduced HMGB1 levels, suggesting HMGB1
Area of Science:
- Endocrinology
- Cardiovascular Research
- Inflammation Biology
Background:
- High-mobility group box 1 (HMGB1) is implicated in systemic inflammation and atherosclerosis.
- Polycystic ovary syndrome (PCOS) is associated with increased cardiovascular risk and endothelial dysfunction.
Purpose of the Study:
- To investigate the relationship between serum HMGB1 levels and endothelial function in women with PCOS.
- To assess the effect of metformin on serum HMGB1 levels and endothelial function in PCOS patients.
Main Methods:
- Serum HMGB1 levels were measured using ELISA in 80 PCOS patients and 80 controls.
- Endothelial function was assessed via high-resolution ultrasound measuring flow-mediated dilation (FMD).
- PCOS patients received metformin (1,500 mg/day) for 3 months.
Main Results:
- Serum HMGB1 levels were significantly higher in PCOS patients compared to controls (24.87 vs. 8.82 ng/ml).
- Metformin treatment significantly reduced HMGB1 levels in PCOS patients.
- Higher HMGB1 levels correlated with increased testosterone and decreased FMD in PCOS patients.
Conclusions:
- Serum HMGB1 levels are elevated and correlated with endothelial dysfunction in PCOS.
- HMGB1 may play a role in the early stages of atherosclerosis in PCOS.
- Metformin therapy may improve endothelial function by reducing HMGB1 levels in PCOS.
Abstract:
High-mobility group box 1 (HMGB1) is newly discovered protein, which play a crucial role in the pathogenesis of systemic inflammation. Recent studies showed that HMGB1 is one of the important pathophysiological mechanisms in the occurrence and development of atherosclerosis. The purpose of the present study was to investigate the relationship between serum HMGB1 levels and endothelial function in patients with polycystic ovary syndrome (PCOS). Eighty newly diagnosed patients with PCOS and eighty normal women of similar age were selected. Metformin treatment (1,500 mg/day) was initiated in all patients for a period of consecutive 3 months. Serum HMGB1 levels were measured by ELISA. High resolution ultrasound was used to measure the brachial artery diameter at rest, after reactive hyperemia (flow-mediated arterial dilation, FMD) and after sublingual glyceryltrinitrate. Serum HMGB1 levels in PCOS were 24.87+/-14.93 ng/ml, which were significantly higher than that in controls (8.82+/-3.55 ng/ml, p<0.01). After 3 months treatment, serum HMGB1 levels decreased significantly (p<0.05). By dividing the distribution of HMGB1 levels into quartiles, serum HMGB1 levels were increased gradually with the increase of testosterone levels (p<0.05), whereas the FMD levels decreased (p<0.05). Multiple stepwise linear regression analysis showed that FMD (estimated coefficient beta=-0.69, p=0.005), testosterone (beta=0.31, p=0.045), TBARS (beta=0.69, p=0.012) and hs-CRP levels (beta=0.68, p=0.001) were significantly associated with HMGB1. The absolute changes in HMGB1 showed a positive correlation with the changes in testosterone (p<0.05) and negative correlation with the changes in FMD (p<0.05) in patients with PCOS during the course of metformin therapy. Serum HMGB1 levels are correlated with endothelial dysfunction in patients with PCOS. Our study suggests that HMGB1 may contribute to the early stage of atherosclerosis in patients with PCOS.
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