Research Progress of Hepcidin in Preeclampsia
YANG Jiani1, YANG Qi1, LUO Xiaoqi1, XU Rongrong2, CUI Hongmei2 *
PE (preeclampsia) is a multi-system disease specific to pregnancy, which seriously threatens the health of both mother and fetus. Its pathogenesis is complex, involving multiple aspects such as abnormal placental function, vascular endothelial injury, inflammatory response, and oxidative stress. In recent years, more and more evidence has shown that iron metabolism disorders, especially iron overload-induced oxidative stress, may play a key role in the pathophysiological process of PE. Hepcidin, as the core regulator of iron metabolism in the body, controls intestinal iron absorption and the release of iron from the reticuloendothelial system by degrading its key target, FPN1 (ferroportin 1). Hepcidin is often highly expressed in PE patients and may be involved in the occurrence and development of PE through mechanisms such as interfering with placental iron transport, exacerbating oxidative stress, and promoting endothelial cell dysfunction, though its expression changes remain controversial. This article aims to systematically review the regulatory mechanism of hepcidin, and the adaptive changes of iron metabolism during normal pregnancy, to focus on discussing the role of abnormal hepcidin levels and hepcidin-mediated iron metabolism disorders in the pathogenesis of preeclampsia, and to analyze the possibility of hepcidin as a potential biomarker and therapeutic target, thereby providing new ideas for the in-depth research and clinical management of PE.
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