Background: Preeclampsia (PE), as a pathological pregnancy process, is still unclear in its precise pathophysiology. The current consensus on PE pathogenesis is that it is an immune‐inflammatory response due to placental dysfunction leading to multiorgan involvement in the mother. Macrophages can polarize into different phenotypes under the influence of distinct microenvironments, secreting various cytokines or chemokines with distinct functions. These phenotypes play roles in either promoting inflammation or facilitating tissue repair. Studies have observed the increase in M1 polarization of decidual macrophages during the occurrence of PE, with this polarization imbalance contributing to the immuno‐inflammatory response involved in placental formation. Therefore, understanding the polarization characteristics of macrophages provides a valuable direction for research related to the prevention and treatment of PE.Methods: Authors searched for related literature on PubMed using the professional terms “preeclampsia” and “macrophage polarization”. The obtained literature was categorized according to its research. Similar articles are summarized in the same sections, which are divided into different small sections according to their specific contents.Results: Different studies have explored the metabolic characteristics, surface markers, secretions, signaling pathways, and functions of different macrophage polarization types, highlighting the critical role of polarization imbalance and excessive inflammatory responses in the development of PE. Intervening in inflammatory responses at the maternal‐fetal interface holds significant value for the prevention and treatment of PE.Conclusion: Understanding the metabolic characteristics of different macrophage polarization types, combined with their polarization imbalance during the development of PE, can facilitate targeted prevention of PE.

Introduction: Pregnancy induces significant physiological changes in the hemostatic system, leading to a hypercoagulable state to prevent postpartum hemorrhage. These adaptations involve alterations in coagulation and fibrinolysis, which can be further modified in complicated pregnancies such as gestational diabetes mellitus (GDM) and preeclampsia (PE). Aim: This study investigated coagulation and fibrinolysis parameters in healthy pregnancies across different gestational stages and compared them to GDM and PE in the third trimester. Methods: In this retrospective study, 293 pregnant women undergoing prenatal check‐ups were enrolled. Coagulation parameters (prothrombin time, PT; activated partial thromboplastin time, APTT; thrombin time, TT; and fibrinogen, FIB) and fibrinolysis parameters (fibrin/fibrinogen degradation products, FDP; D‐dimer; plasminogen activator inhibitor‐1, PAI‐1; tissue plasminogen activator, tPA; and plasmin‐α2‐plasmin inhibitor complex, PIC) were measured and compared across groups: non‐pregnant controls, healthy pregnancies (first trimester, third trimester, delivery), GDM, and PE. Results: In normal pregnancy, all gestational stages showed significantly shortened PT, APTT, and TT and elevated FIB, FDP, D‐dimer, PAI‐1, and tPA compared to non‐pregnant controls. FDP and D‐dimer increased progressively with gestation. Compared to the third trimester, GDM was characterized by significantly higher PAI‐1 and tPA but lower PIC, whereas PE was characterized by significantly higher PAI‐1 and PIC, prolonged APTT, and lower tPA. Furthermore, among healthy women at delivery and those with GDM, overweight and obesity were associated with significantly increased PAI‐1 levels. Conclusion: As pregnancy progresses, enhanced coagulation with hypofibrinolysis occurs in normal pregnancy, and further hypofibrinolysis is the primary thrombotic driver in GDM and obesity. PE presents a more complex alteration in both coagulation and fibrinolytic pathways.

Aspirin prevents preterm birth in some women with preeclampsia but not others, yet no longitudinal multi-indicator study has examined subtype differences in aspirin response. We aimed to identify subtypes most likely to benefit. In this retrospective cohort of 53,362 deliveries (4505 preeclamptic women), we applied a two-stage machine learning framework using 15 indicators (14 laboratory tests plus systolic blood pressure) from two-time windows: before 16 weeks and within 2 weeks before delivery. A long short-term memory autoencoder with K-means clustering identified subtypes, and causal forest estimated the average treatment effect of aspirin on preterm birth (<37 weeks) for each subtype, adjusted for confounders. Five stable subtypes were identified (silhouette coefficient 0.542; mean adjusted Rand index 0.903). One subtype (n = 345), characterised by mild liver enzyme elevation and coagulation abnormalities in late pregnancy, had the highest preterm birth rate (57.7%) and ICU admission rate (9.6%), and showed the largest aspirin-associated reduction in preterm birth (ATE −0.026, 95% CI: −0.032 to −0.021), consistent across 70/30 splits. Sensitivity analyses using 34 indicators confirmed similar effects (ATE −0.027, 95% CI: −0.031 to −0.023), while no benefit was observed in non-preeclamptic women. These findings suggest that aspirin prophylaxis may be associated with a greater reduction in preterm birth in this preeclampsia subtype, but further validation is required.