Preeclampsia (PE) is a pregnancy-specific disorder that impacts 2-10% of pregnant mothers and causes significant maternal and fetal death. Clinical symptoms usually arise after 20 weeks of gestation, but evidence suggests that the pathophysiological mechanisms start much earlier. PE is caused by a combination of factors such as abnormal placentation, systemic inflammation, oxidative stress, and, most importantly, an imbalance between angiogenic mediators (VEGF and PlGF) and anti-angiogenic factors (sFlt-1 and sEng). This imbalance leads to endothelial dysfunction, decreased uteroplacental perfusion, and poor pregnancy outcomes. This warrants an ideal therapeutic module would that is safe during pregnancy, reduce placental anti-angiogenic factor release, and restore endothelial function and angiogenesis. . Metformin, a widely used biguanide with an established safety profile in pregnancy, has emerged as a promising treatment candidate due to its beneficial effects on cellular metabolism, inflammation, oxidative stress, and endothelial function. , making it a promising option for the prevention and management of preeclampsia. This study thus evaluates the possible function of metformin in preeclampsia prevention, with a focus on its effects on angiogenic balance, oxidative stress and other major pathogenic pathways.
Keywords: Angiogenesis; Anti-angiogenic; Endothelial dysfunction; Hypertension; Metformin; Preeclampsia.
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