时间标签：数据日期 2026-10-31 · 生成时间 2026-11-01 05:30（Asia/Shanghai）｜ 检索窗口 PubMed edat 2026/10/28–2026/10/31 ｜ 情报发生日期 2026-10-31
研究问题
However, male fetuses may have greater susceptibility to early-life effects but be less susceptible to insults in the uterus (; ).；Although miR-543 has been implicated in endothelial cell (EC) survival and tube formation in cancer models (), the precise downstream targets and functional pathways through which it orchestrates this sex-dimorphic angiogenic impairment in placental development remain entirely unknown.；To address this gap, we performed in silico target prediction and bioinformatics pathway analysis to screen for downstream effectors of miR-543 and examined how these targets and their signaling cascades regulate EC-mediated angiogenesis.
方法
All recruited pregnancies provided informed consent.；The participants were categorized into an FGR group, defined by a birth weight below the 10th percentile for gestational age (), and a control group comprising pregnancies with normal birth weight, with each group consisting of 10 male and female participants.；The exclusion criteria were as follows: 1) pregnancy-related complications, such as preeclampsia or gestational diabetes; 2) gestational age less than 37 weeks; and 3) multiple pregnancies.；This study was approved by the hospital ethics committee (Approval ID: 20210030) and registered with the Chinese Clinical Trial Registry (Registration Number: ChiCTR2100043159) on 7th February 2021.
核心结论
Consistent with our previous sequencing data identifying miR-543 as the most significantly dysregulated miRNA in female FGR placentas (), qRT-PCR validation confirmed a marked downregulation of miR-543 in female FGR placentas compared with controls (p = 0.008) ().；No significant difference was observed in male FGR placentas compared with male controls (p = 0.126).；These findings confirm sex-specific dysregulation of placental miR-543 in FGR. ‖ 结论：Our experimental data recapitulated these findings, showing that inhibition of PI3K signaling markedly reduced caspase-3 expression in HUVECs, confirming that the PI3K/AKT/mTOR pathway mediated adaptive cytoprotective effects in endothelial cells.
局限
However, this study has several limitations.；The relatively small sample size may restrict the statistical power.
对本项目的价值
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全文来源
PMC JATS 全文（正文 27,511 字符，已过标题/DOI 逐字归属校验）
原文题录
- 英文标题：miRNA-543 attenuates placental angiogenesis in female fetal growth restriction by targeting ANGPT2 and inhibiting the PI3K/AKT/mTOR pathway.
- 期刊与标识：Front Cell Dev Biol · PMID 42964304 · DOI 10.3389/fcell.2026.1912518
A 级证据分级：A 级（同行评议人体研究）
本文属人体研究证据，但需注意：观察性或小样本干预的结论不等于已证实临床获益；效应量与长期安全性仍需更大规模、更长随访的试验验证。
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