Department of Obstetrics, Ganzhou People's Hospital, Ganzhou, Jiangxi, China.
Department of Obstetrics and Gynecology, Ganzhou People's Hospital, Ganzhou, Jiangxi, China.
Clinics (Sao Paulo). 2022 Sep 7;77:100079. doi: 10.1016/j.clinsp.2022.100079. eCollection 2022.
Preterm birth is the leading cause of infant mortality. The mechanisms that instigate preterm birth remain elusive and this makes it difficult to predict or prevent preterm birth. In this study, the authors found that SP-A induced pathological damage to the placenta and promoted preterm birth. Through mechanism, SP-A promoted the expression of STOX1 which further promoted the oxidative stress in the placenta by inhibiting the activities of a series of antioxidant enzymes including SOD, CAT and GSH-Px. SP-A also induced dysregulation of arginine metabolism by inhibiting NOS2 and ARG2. Overexpression of STOX1 aggravated SP-A induced oxidative stress, pathological damage, and preterm birth, whereas knockdown of STOX1 alleviated SP-A induced oxidative stress, pathological damage and preterm birth. The present study uncovers that SP-A induces preterm birth by promoting oxidative stress via upregulating STOX1, which provides new targets for the prediction and prevention of preterm birth.
早产是婴儿死亡的主要原因。引发早产的机制仍难以捉摸,这使得预测或预防早产变得困难。在这项研究中,作者发现 SP-A 诱导胎盘发生病理性损伤并促进早产。通过机制研究发现,SP-A 促进 STOX1 的表达,通过抑制一系列抗氧化酶(包括 SOD、CAT 和 GSH-Px)的活性,进一步促进胎盘的氧化应激。SP-A 还通过抑制 NOS2 和 ARG2 诱导精氨酸代谢失调。过表达 STOX1 加重了 SP-A 诱导的氧化应激、病理性损伤和早产,而 STOX1 的敲低则减轻了 SP-A 诱导的氧化应激、病理性损伤和早产。本研究揭示 SP-A 通过上调 STOX1 促进氧化应激诱导早产,为早产的预测和预防提供了新的靶点。