Expression of Angiogenic and Endothelial Dysfunction Genes in Gestational Diabetes Mellitus: Focus on VEGF-A and ALOX12

Document Type : Original Article

Authors

1 Prenatal Diagnosis and Fetal Medicine Department, Human Genetics and Genome Research Institute, National Research Centre Cairo, Egypt.

2 Medical Molecular Genetics, National Research centre

3 1 Prenatal Diagnosis and Fetal Medicine Department, Human Genetics and Genome Research Institute, National Research Centre Cairo, Egypt.

Abstract

Abstract

Background: Gestational diabetes mellitus (GDM) is a prevalent pregnancy complication involving hyperglycemia, which can disrupt placental angiogenesis and endothelial function, increasing maternal and fetal risks.

Aim: This study evaluated the expression levels of vascular endothelial growth factor A (VEGF-A) and arachidonate 12-lipoxygenase (ALOX12) genes in pregnant women diagnosed with GDM compared to healthy controls, and explored their associations with clinical and biochemical parameters.

Methods: A case-control study was performed included 200 pregnant women (100 with GDM and 100 controls). Gene expression levels of VEGF-A and ALOX12 were quantified in maternal plasma using quantitative real-time PCR (qRT-PCR). Relevant clinical and biochemical parameters were also recorded.

Results: Both VEGF-A and ALOX12 were significantly upregulated in the GDM group. VEGF-A expression was 2.65 ± 1.8 in GDM vs. 1.72 ± 1.3 in controls (95% CI: 0.461–1.38; P < 0.05). ALOX12 expression was 0.63 ± 0.6 in GDM vs. 0.36 ± 0.3 in controls (95% CI: 0.128–0.415; P < 0.05). Statistical analysis revealed a significant correlation between VEGF-A expression with urea and total cholesterol (P < 0.05), while ALOX12 expression correlated with HDL levels (P = 0.04).

Conclusion: The increased expression of VEGF-A and ALOX12 in GDM suggests their role in abnormal angiogenesis and vascular dysfunction. Their associations with metabolic markers highlight their potential as biomarkers for vascular risk and GDM-related complications.

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Articles in Press, Accepted Manuscript
Available Online from 10 September 2025
  • Receive Date: 20 July 2025
  • Revise Date: 28 August 2025
  • Accept Date: 10 September 2025