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

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.