Table 1.
Summary of modeling methods, strengths and limitations, and applicability of the PAS mouse models.
| Model | Approaches | Strengths | Limitations | Applicability | Reference |
|---|---|---|---|---|---|
| Surgery-induced models | Uterine incision | Accompanied by impaired immune and inflammatory environment in the maternal–fetal interface | Invasive surgery, possibly embryonic resorption | Suitable for the research of disordered immune and inflammation in maternal–fetal interface of PAS | (50) |
| Cesarean section | Damage to the myometrium, simulate the most essential PAS risk factor CS | Invasive surgery, disturb the estrous cycle | More suitable to investigate the pathomechanism of PAS in the aspect of myometrium abnormalities | (68) | |
| Dilation & curettage | Surgical procedures before pregnancy, mostly impair the endometrium | Invasive repeated operation | More suitable to investigate the pathomechanism of PAS in the aspect of endometrial abnormalities | (68) | |
| Genetically modified models | Simulate the decidual deficiency (Gab3 knockout) | High stability theoretically, non-invasive, pinpoint the role of specific gene in PAS progress | The modeling success rate might be relatively low, possible embryonic death, lower birth rates | Suitable to investigate the pathomechanism of PAS in aspect of decidua deficiency, also to explore the mechanism of uNK cells in the PAS | (74) |
| Simulate the excessive invasion of EVT (MARVELD1knockout) | Simulate the excessive invasion of trophoblast cells of PAS | (75) | |||
| Simulate the invasion of the mature placenta (adrenomedullin knockdown) | Optimal tool to study the placental vascular remodeling in PAS, also suitable to develop the angiogenesis-related marker in serum. | (76) |