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<p>We aimed to examine how placental dysfunction and impaired mitochondrial fusion/fission balance correlate with preeclampsia (PE) in human placentas, shedding light on the underlying etiology of PE. Twenty-eight pregnant women who received antenatal care at the Obstetrics Medical Center of Weifang People’s Hospital between November 2024 and May 2025. They were divided into a PE group (<i>n</i> = 14) and a normal control group (<i>n</i> = 14). Placental tissues from pregnant women with PE or with healthy control were analyzed. Compared to controls, the PE group exhibited impaired placental function (evidenced by decreased PlGF and increased sFlt-1) and disrupted mitochondrial dynamics (characterized by reduced MFN1/2 and elevated p-DRP1). These alterations were accompanied by increased oxidative stress and apoptosis, alongside decreased ATP production. Imbalanced mitochondrial fusion/fission may contribute to placental dysfunction through mechanisms involving oxidative stress, disturbed energy metabolism, and cell apoptosis, leading to the occurrance of PE.</p>

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Imbalanced mitochondrial fusion/fission in human placenta: a potential link to preeclampsia

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年6月26日

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  • Jianying Liu,
  • Yujing Xu,
  • Hong Sun,
  • Shasha Yu,
  • Rong Hou,
  • Ruofan Wang,
  • Qian Li,
  • Xiaoyi Yin,
  • Yuchun Zhu,
  • Guanglei Wang

摘要

We aimed to examine how placental dysfunction and impaired mitochondrial fusion/fission balance correlate with preeclampsia (PE) in human placentas, shedding light on the underlying etiology of PE. Twenty-eight pregnant women who received antenatal care at the Obstetrics Medical Center of Weifang People’s Hospital between November 2024 and May 2025. They were divided into a PE group (n = 14) and a normal control group (n = 14). Placental tissues from pregnant women with PE or with healthy control were analyzed. Compared to controls, the PE group exhibited impaired placental function (evidenced by decreased PlGF and increased sFlt-1) and disrupted mitochondrial dynamics (characterized by reduced MFN1/2 and elevated p-DRP1). These alterations were accompanied by increased oxidative stress and apoptosis, alongside decreased ATP production. Imbalanced mitochondrial fusion/fission may contribute to placental dysfunction through mechanisms involving oxidative stress, disturbed energy metabolism, and cell apoptosis, leading to the occurrance of PE.