TGF-β2 drives lipid droplet accumulation in chondrocytes through the TβRI/p-smad3/fabp5 axis.

Recurrent spontaneous abortion (RSA) refers to ≥2 consecutive pregnancy losses with the same sexual partner before 28 weeks of gestation, including adverse outcomes such as spontaneous abortion, embryonic arrest, and biochemical pregnancy. Its incidence rate is approximately 1%–5% (, ), showing a substantial upward trend with advancing maternal age and an increasing number of previous abortions (). RSA can cause long-term complications such as endometrial damage, endocrine disorders, and pelvic infections, as well as psychological disorders, including anxiety and depression, placing a heavy burden on families and society. Thus, it has become a major public health issue in reproductive health. The etiology of RSA involves the interaction of multiple factors, including genetic, anatomical, endocrine, autoimmune, infectious, and thrombophilia factors. Among these, embryonic chromosomal abnormalities account for > 50% of early miscarriages, whereas uterine anatomical abnormalities increase the risk of miscarriage by interfering with embryonic implantation and development (). Despite the ongoing in-depth etiological research, the underlying cause remains undetermined in 40%–50% of RSA cases, complicating clinical management and considerably increasing the risk of recurrent pregnancy loss (). Unlike in infertility, the management of which focuses on achieving pregnancy, the core clinical objectives of RSA treatment are to maintain pregnancy to term, reduce the miscarriage rate, and increase the live birth rate. Therefore, early identification of risk factors and the implementation of stratified interventions are crucial. A prothrombotic state, characterized by an imbalance in the anticoagulant–fibrinolytic system and hypercoagulability, can trigger microthrombosis in the placental microcirculation, leading to inadequate placental perfusion, embryonic ischemia and hypoxia, and thereby subsequent pregnancy loss (). Moreover, thyroid dysfunction considerably increases the risk of adverse pregnancy outcomes by disrupting endocrine homeostasis, affecting luteal function and placental hormone synthesis, and compromising maternal–fetal immune tolerance (). Early pregnancy markers, such as coagulation function, platelet aggregation, thyroid function, homocysteine, and antinuclear antibodies, represent routine non-invasive obstetric tests that can comprehensively assess the mother’s pathophysiological status ().