On February 11, 2026, the research team led by Academician Hefeng Huang, Academician of the Chinese Academy of Sciences, from the Center for Reproductive Medicine at Zhejiang University’s International Institutes of Medicine (ZJU-IIM) published new findings in Advanced Science.
Gestational hyperglycemia is a common pregnancy complication that threatens maternal and fetal health and increases the risk of fetal growth restriction (FGR), the core clinical issue addressed in this study.
Using a hyperglycemic mouse model, the research team found that gestational hyperglycemia impairs the formation of placental syncytiotrophoblasts and reduces placental function, thereby leading to fetal growth restriction. This phenotype arises from impaired trophoblast cell fusion.
Transcriptome sequencing and functional experiments confirmed that Tim1 acts as a key regulator of trophoblast fusion. Hyperglycemia suppresses Tim1 expression via oxidative stress (ROS), and Tim1-deficient mice recapitulate the fetal growth restriction phenotype caused by gestational hyperglycemia.
Experiments demonstrated that the antioxidants N-Acetylecyseine (NAC) and Coenzyme Q10 (CoQ10) can reverse the high glucose-induced downregulation of Tim1 and the impairment of cell fusion. Clinical sample analysis further confirmed that Tim1 levels are significantly reduced in placental tissues from patients with pre-pregnancy diabetes complicated by FGR, validating the clinical relevance of this work
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This study reveals for the first time the oxidative stress–Tim1–trophoblast fusion regulatory axis, offers a potential antioxidant intervention strategy, and provides a theoretical and translational basis for the clinical management of gestational hyperglycemia-related FGR.
Link to the full article:
https://doi.org/10.1002/advs.202508686
