Preeclampsia is a common and severe pregnancy-related disease, affecting 2.7 %-8.2 % of pregnant women. It is characterized by the onset of high blood pressure (≥140 mm Hg systolic or ≥ 90 mm Hg diastolic) and proteinuria after 20 weeks of pregnancy, which increases the risk of preterm birth, cardiovascular disease, and kidney disease in pregnant women, and the mortality of mother and fetus [1]. Studies suggest that preeclampsia originates from inadequate blood perfusion caused by the invasion failure of extravillous trophoblasts (EVTs) in the uterine endometrium and the failure remodeling of uterine spiral arteries, which occurs around 8–10 weeks of pregnancy [2]. Inadequate trophoblastic invasion leads to widespread inflammation and endothelial impairment, such as increased platelet aggregation and placental infarcts, due to an imbalance of angiogenic and antiangiogenic proteins. To overcome the damage processes, a long-term use of low-dose aspirin, inactivating the cyclooxygenase-1 enzyme and suppressing the production of prostaglandins and thromboxane, was applied for early intervention in the pregnant under preeclampsia risk [3]. However, it fails to ameliorate the levels of placental growth factor (PlGF)and placental soluble fms-like tyrosine kinase 1 (sFlt1), nor does it improve placental blood flow, as assessed from the perspective of placental pathology [4,5]. Therefore, exploring other potential drugs is of great significance for early intervention in the early stages of preeclampsia. A systematic evaluation of the pre-eclampsia drugs, dietary supplements was conducted, revealing 153 candidates for pre-eclampsia intervention, 7 of which were classified as high potential (prevention: esomeprazole, l-arginine, chloroquine, vitamin D and metformin; treatment: sulfasalazine and metformin) and 8 as medium potential (prevention: probiotic lactobacilli, dalteparin, selenium and omega-3 fatty acid; treatment: sulforaphane, pravastatin, rosuvastatin and vitamin B3) [6]. Recently, statins (pravastatin) and metformin have been explored in recent trials or studies for preeclampsia early intervention [[7], [8], [9], [10]]. However, different from these generative materials for amelioration, rosiglitazone, a synthetic peroxisome proliferator-activated receptor gamma (PPARγ) agonist already used in humans for the treatment of type 2 diabetes, has the potential to intervene in key biological processes during placentation through activation of PPARγ. Specifically, rosiglitazone activates PPARγ, a nuclear receptor that regulates genes involved in lipid transport and metabolism, glucose homeostasis, and inflammatory responses. Notably, PPARγ levels have been reported to be reduced in early-onset preeclamptic placentas compared to the normal, suggesting that PPARγ activation might counteract a disease-related deficiency [11]. By modulating PPARγ activity, rosiglitazone may influence critical aspects of placental development and function, including trophoblast differentiation, nutrient transport, vascularization, and immunomodulation. Further investigation into the effects of rosiglitazone on the placenta may uncover new therapeutic opportunities to improve pregnancy outcomes, including preeclampsia. However, the pregnancy toxicity of rosiglitazone remains undefined since animal studies have shown no side effects in implantation or embryonic growth during early pregnancy in rats or rabbits although it does cause fetal death and growth retardation in late-term rats and rabbits when used long-term at doses of 3 mg/kg and 100 mg/kg, respectively, which equals to 20 times and 75 times the maximum recommended dose for humans. Moreover, rosiglitazone is non-toxic on the placenta, embryos/fetuses, or offspring when administered at a dose of 0.2 mg/kg/day in rats and 15 mg/kg/day in rabbits, four times the maximum recommended dose for humans [12]. This gives an application opportunity for the clinical practice of rosiglitazone. Therefore, we performed a thorough literature review based on Google Scholar, PubMed, and Web of Science using the combined or not keywords: 'PPARγ', ‘Peroxisome proliferator-activated receptor gamma’, 'rosiglitazone', 'preeclampsia', and ‘placenta’. As a narrative review, it focuses on in vitro, animal, and clinical reports of PPARγ/rosiglitazone in preeclampsia, published up to May 2025. Only English-language studies relevant to the theme of this review were included. This review aims to provide an overview of the research advances on the potential therapeutic use of rosiglitazone as an early intervention for preeclampsia.