ULK2 deficiency stratifies autophagy-driven molecular subtypes and exacerbates trophoblasts apoptosis in preeclampsia.

Journal: Placenta
Published Date:

Abstract

INTRODUCTION: Preeclampsia (PE), a placenta-originated hypertensive disorder of pregnancy, lacks targeted therapies despite its significant contribution to maternal and fetal morbidity. Emerging evidence implicates autophagy dysregulation in PE pathogenesis, though its molecular heterogeneity remains unexplored. This study aims to investigate autophagy-related molecular subtypes in PE and identify ULK2 key regulators linking autophagic imbalance to placental dysfunction.

Authors

  • Jianfeng Gan
    Obstetrics and Gynecology Hospital of Fudan University, Fangxie Road 419, Shanghai, China; Shanghai Key Laboratory of Female Reproductive Endocrine-Related Diseases, Shanghai, China.
  • Wenhan Zhou
    Obstetrics and Gynecology Hospital of Fudan University, Fangxie Road 419, Shanghai, China; Shanghai Key Laboratory of Female Reproductive Endocrine-Related Diseases, Shanghai, China.
  • Huanqiang Zhao
    Affiliated Shenzhen Maternity & Child Healthcare Hospital, Southern Medical University, Shenzhen, China.
  • Jiejie Shao
    Obstetrics and Gynecology Hospital of Fudan University, Fangxie Road 419, Shanghai, China; Shanghai Key Laboratory of Female Reproductive Endocrine-Related Diseases, Shanghai, China.
  • Yutong Cui
    Shanghai Funiirst Maternity and Infant Hospital, Tongji University School of Medicine, Shanghai, China.
  • Suwen Wu
    Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
  • Huangfang Xu
    Department of Gynecology, The Second Affiliated Hospital, Zhejiang University School of Medicine, Zhejiang University, Hangzhou, China.
  • Yinan Wang
  • Qiongjie Zhou
    Obstetrics and Gynecology Hospital, Fudan University, Shanghai, China.
  • Xiaotian Li
    Obstetrics and Gynecology Hospital, Fudan University, Shanghai, China.