Background <p>Polycystic Ovary Syndrome (PCOS) is a complex endocrine syndrome impacting women during their reproductive phase of life and is increasingly recognized for its association with cardiovascular comorbidities, particularly hypertension. Despite its clinical significance, the hypertensive PCOS (H-PCOS) remains poorly characterized at the molecular level.</p> Methods and results <p>The current study aimed to investigate the gene expression profiles of <i>Endothelin-1</i> (<i>ET-1</i>) and Cytochrome P450 family 11subfamilly A member 1(<i>CYP11A1)</i> to elucidate their potential roles in the vascular and metabolic disturbances observed in H-PCOS. A total of 69 Kurdish women aged 18 to 53 were enrolled and classified into three groups: PCOS without hypertension, hypertensive PCOS, and healthy controls. Using qRT-PCR, we measured gene expression levels and assessed serum gonadotropin hormones and lipid profiles. ROC analysis showed that <i>ET-1</i> (AUC = 0.8667, <i>p</i> = 0.0003) and <i>CYP11A1</i> (AUC = 0.7667, <i>p</i> = 0.009) had significant diagnostic value, while fold-change analysis revealed approximately 13.5-fold and 82-fold increases, respectively, in H-PCOS patients compared with controls and non-hypertensive PCOS, confirming a statistically robust upregulation of both genes. Gene expression levels and clinical measurements including body mass index (BMI), Luteinizing Hormone to Follicle-Stimulating Hormone (LH/FSH) ratio, and Mean Arterial Pressure (MAP) were strongly correlated. H-PCOS was clearly separated from other groups using receiver operating characteristic (ROC) analysis for <i>ET-1</i>, <i>CYP11A1</i>, BMI, and the Total Cholesterol to High Density Lipoprotein-Cholesterol (TC/HDL-C) ratio.</p> Conclusion <p>These findings highlight that endocrine and vascular irregularities are key features of genetic profile of H-PCOS. <i>ET-1</i> and <i>CYP11A1</i> can be used as potential biomarkers to better guide H-PCOS diagnosis of hypertension and therapy.</p>

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Molecular signatures of hypertension in polycystic ovary syndrome: Endothelin-1 and CYP11A1 as biomarkers of vascular and metabolic dysfunction

  • Mohammed-Ridha Hosein,
  • Zjwan Housein

摘要

Background

Polycystic Ovary Syndrome (PCOS) is a complex endocrine syndrome impacting women during their reproductive phase of life and is increasingly recognized for its association with cardiovascular comorbidities, particularly hypertension. Despite its clinical significance, the hypertensive PCOS (H-PCOS) remains poorly characterized at the molecular level.

Methods and results

The current study aimed to investigate the gene expression profiles of Endothelin-1 (ET-1) and Cytochrome P450 family 11subfamilly A member 1(CYP11A1) to elucidate their potential roles in the vascular and metabolic disturbances observed in H-PCOS. A total of 69 Kurdish women aged 18 to 53 were enrolled and classified into three groups: PCOS without hypertension, hypertensive PCOS, and healthy controls. Using qRT-PCR, we measured gene expression levels and assessed serum gonadotropin hormones and lipid profiles. ROC analysis showed that ET-1 (AUC = 0.8667, p = 0.0003) and CYP11A1 (AUC = 0.7667, p = 0.009) had significant diagnostic value, while fold-change analysis revealed approximately 13.5-fold and 82-fold increases, respectively, in H-PCOS patients compared with controls and non-hypertensive PCOS, confirming a statistically robust upregulation of both genes. Gene expression levels and clinical measurements including body mass index (BMI), Luteinizing Hormone to Follicle-Stimulating Hormone (LH/FSH) ratio, and Mean Arterial Pressure (MAP) were strongly correlated. H-PCOS was clearly separated from other groups using receiver operating characteristic (ROC) analysis for ET-1, CYP11A1, BMI, and the Total Cholesterol to High Density Lipoprotein-Cholesterol (TC/HDL-C) ratio.

Conclusion

These findings highlight that endocrine and vascular irregularities are key features of genetic profile of H-PCOS. ET-1 and CYP11A1 can be used as potential biomarkers to better guide H-PCOS diagnosis of hypertension and therapy.