Abstract:

Fetal growth restriction (FGR) is an important contributor of perinatal morbidity and mortality. Its pathogenesis is complex, involving multiple factors at the fetal, maternal, and placental levels. As a core organ for material exchange and endocrine regulation between the mother and the fetus, abnormal placental structure and function play a crucial role in the pathogenesis of FGR. In recent years, studies have revealed that the occurrence of FGR is not only accompanied by macroscopic morphological changes such as reduced placental volume and disrupted villous tree structure but is also deeply associated with dysfunctions in trophoblast proliferation and differentiation, leading to insufficient remodeling of the spiral arteries. Advances in epigenetics have shown that the occurrence of FGR is accompanied by abnormal genomic imprinting in the placenta, alterations in DNA methylation patterns, and dysregulated expression of various microRNAs. These changes can contribute to the development of FGR by regulating placental development, angiogenesis, and cellular stress responses. With the development of multi-omics, research on the placental etiology of FGR is deepening to more refined cellular and molecular levels. This review summarizes the research progress of placental morphology, cell functional studies, and epigenetics in FGR, aiming to enhance the understanding of its pathological mechanisms and provide a scientific basis for early identification and precise intervention.

Key words: Fetal growth retardation, Placenta, Trophoblasts, Uterine artery, Genomic imprinting, Epigenomics, MicroRNAs