Preeclampsia is a serious pregnancy complication characterized by hypertension and organ dysfunction. The pathophysiology of preeclampsia involves a two-stage model: impaired uteroplacental perfusion and systemic endothelial dysfunction. Fetal microchimerism, where fetal cells persist in maternal tissues and circulation, links placental dysfunction to maternal complications. Hormones, complements, and cytokines play crucial roles in immune responses, arterial remodeling, and endothelial function. Soluble HLA-G, involved in maternal-fetal immune tolerance, is reduced in preeclampsia. Hypoxia-inducible factor 1-alpha (Hif-α) dysregulation leads to placental abnormalities and preeclampsia-like symptoms. Matrix metalloproteinases (MMPs), endothelin (ETs), chemokines, and cytokines contribute to defective trophoblast invasion, endothelial dysfunction, and inflammation. Genetic factors, including circular RNAs (circRNAs), microRNAs (miRNAs), and long non-coding RNAs (lncRNAs), influence trophoblast function and angiogenesis. CD31+ cells and biomarkers like MMPs, sHLA-G, and hCG hold promise for predicting preeclampsia and its complications. Therapeutic interventions targeting peroxisome PPAR-γ and endothelin receptors show potential in mitigating preeclampsia-related complications. The review highlights the multifactorial etiology and pathogenesis of preeclampsia, emphasizing the importance of identifying novel biomarkers and therapeutic targets for early diagnosis and effective management.Preeclampsia is a serious pregnancy complication characterized by hypertension and organ dysfunction. The pathophysiology of preeclampsia involves a two-stage model: impaired uteroplacental perfusion and systemic endothelial dysfunction. Fetal microchimerism, where fetal cells persist in maternal tissues and circulation, links placental dysfunction to maternal complications. Hormones, complements, and cytokines play crucial roles in immune responses, arterial remodeling, and endothelial function. Soluble HLA-G, involved in maternal-fetal immune tolerance, is reduced in preeclampsia. Hypoxia-inducible factor 1-alpha (Hif-α) dysregulation leads to placental abnormalities and preeclampsia-like symptoms. Matrix metalloproteinases (MMPs), endothelin (ETs), chemokines, and cytokines contribute to defective trophoblast invasion, endothelial dysfunction, and inflammation. Genetic factors, including circular RNAs (circRNAs), microRNAs (miRNAs), and long non-coding RNAs (lncRNAs), influence trophoblast function and angiogenesis. CD31+ cells and biomarkers like MMPs, sHLA-G, and hCG hold promise for predicting preeclampsia and its complications. Therapeutic interventions targeting peroxisome PPAR-γ and endothelin receptors show potential in mitigating preeclampsia-related complications. The review highlights the multifactorial etiology and pathogenesis of preeclampsia, emphasizing the importance of identifying novel biomarkers and therapeutic targets for early diagnosis and effective management.