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Peer-reviewedCC BY 4.0Advanced Science

Maternal Hyperglycemia Disrupts Cerebral Cortex Development Through the Foxp1‐Dll1‐Notch Axis

  • Longkai He1,2
  • Ya Jin1
  • Guosheng Liu1
  • Hao Liu1
  • Xinyi Zhu3
  • Weipeng Xu1
  • Wei Li4
  • Meiyao He3
  • Yao Shen3
  • Bingxiao Li1
  • Xuesong Yang3
  • Xiaoyu Wang3
1 more authors
  • Shasha Han1
4 affiliations
  1. 1Division of Neonatology Department of Pediatrics The First Affiliated Hospital of Jinan University Jinan University Guangzhou China
  2. 2Division of Neonatology and Center for Newborn Care Guangzhou Women and Children’s Medical Center Guangzhou Medical University Guangzhou China
  3. 3Department of Histology and Embryology Key Laboratory for Regenerative Medicine of the Ministry of Education College of Medicine Jinan University Guangzhou China
  4. 4Dongguan Binhaiwan Central Hospital (Dongguan Hospital‐Nanfang Hospital Southern Medical University) Dongguan China
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Abstract

Maternal hyperglycemia is associated with adverse neurodevelopmental outcomes in offspring, but the mechanisms by which it affects fetal brain development remain incompletely understood. Using a mouse model of pregestational diabetes mellitus (PGDM), we found that maternal hyperglycemia was associated with reduced cortical thickness and altered cortical lamination. These abnormalities were accompanied by changes in neural stem cell differentiation and asymmetric division, as well as impaired neuronal migration and dendritic development. Transcriptomic analysis identified the transcription factor Foxp1 as markedly downregulated in the PGDM embryonic cortex. Restoring Foxp1 expression in vivo substantially alleviated the observed cortical abnormalities. Mechanistic experiments showed that Foxp1 represses transcription of the Notch ligand Delta‐like 1 (Dll1) and attenuates Notch signaling. Together, these findings implicate the Foxp1–Dll1–Notch axis as one pathway contributing to disrupted corticogenesis in the PGDM model and provide insight into how an adverse intrauterine metabolic environment affects embryonic brain development.

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Cite

BibTeXRIS
BibTeX
@article{he2026maternal,
  title = {{Maternal Hyperglycemia Disrupts Cerebral Cortex Development Through the Foxp1‐Dll1‐Notch Axis}},
  author = {Longkai He and Ya Jin and Guosheng Liu and Hao Liu and Xinyi Zhu and Weipeng Xu and Wei Li and Meiyao He and Yao Shen and Bingxiao Li and Xuesong Yang and Xiaoyu Wang and Shasha Han},
  journal = {Advanced Science},
  year = {2026},
  month = oct,
  doi = {10.1002/advs.78305},
  url = {https://doi.org/10.1002/advs.78305},
  note = {CC BY 4.0},
}
RIS
TY  - JOUR
TI  - Maternal Hyperglycemia Disrupts Cerebral Cortex Development Through the Foxp1‐Dll1‐Notch Axis
AU  - Longkai He
AU  - Ya Jin
AU  - Guosheng Liu
AU  - Hao Liu
AU  - Xinyi Zhu
AU  - Weipeng Xu
AU  - Wei Li
AU  - Meiyao He
AU  - Yao Shen
AU  - Bingxiao Li
AU  - Xuesong Yang
AU  - Xiaoyu Wang
AU  - Shasha Han
PY  - 2026
DA  - 2026/10/26
JO  - Advanced Science
DO  - 10.1002/advs.78305
UR  - https://doi.org/10.1002/advs.78305
AB  - Maternal hyperglycemia is associated with adverse neurodevelopmental outcomes in offspring, but the mechanisms by which it affects fetal brain development remain incompletely understood. Using a mouse model of pregestational diabetes mellitus (PGDM), we found that maternal hyperglycemia was associated with reduced cortical thickness and altered cortical lamination. These abnormalities were accompanied by changes in neural stem cell differentiation and asymmetric division, as well as impaired neuronal migration and dendritic development. Transcriptomic analysis identified the transcription factor Foxp1 as markedly downregulated in the PGDM embryonic cortex. Restoring Foxp1 expression in vivo substantially alleviated the observed cortical abnormalities. Mechanistic experiments showed that Foxp1 represses transcription of the Notch ligand Delta‐like 1 (Dll1) and attenuates Notch signaling. Together, these findings implicate the Foxp1–Dll1–Notch axis as one pathway contributing to disrupted corticogenesis in the PGDM model and provide insight into how an adverse intrauterine metabolic environment affects embryonic brain development.
SN  - 2198-3844
ER  -