已发表论文

脂肪酸转运蛋白 CD36 促进子痫前期氧化低密度脂蛋白诱导的血管内皮细胞衰老

 

Authors Xiao Y, Tao M, Yu Y, Bai R, Zhuang Y, Huang Q, He J, Lin Z, Gao M, Li J, Wang Y, Xu Y, Shen X, Huang Z, Yao Y, Chen Z, Chen Q, Wang Z 

Received 10 June 2025

Accepted for publication 9 September 2025

Published 16 September 2025 Volume 2025:18 Pages 12801—12816

DOI https://doi.org/10.2147/JIR.S538337

Checked for plagiarism Yes

Review by Single anonymous peer review

Peer reviewer comments 4

Editor who approved publication: Dr Adam Bachstetter

Yanxuan Xiao,1,2,* Maliang Tao,3,* Yiqi Yu,1,* Ruiyan Bai,1,2 Yunting Zhuang,1,2 Qiuyu Huang,1 Jiexing He,1 Zeshan Lin,1,2 Mingze Gao,1 Jiaqi Li,1 Yuting Wang,1 Yao Xu,1 Xinyang Shen,1 Zhenqin Huang,1 Yuan Yao,1 Zhiyong Chen,1 Qian Chen,1 Zhijian Wang1,4 

1Department of Obstetrics and Gynecology, Nanfang Hospital, Southern Medical University, Guangzhou, 510515, People’s Republic of China; 2School of Nursing, Southern Medical University, Guangzhou, 510515, People’s Republic of China; 3Department of Laboratory Medicine, Nanfang Hospital, Southern Medical University, Guangzhou, 510515, People’s Republic of China; 4Department of Obstetrics and Gynecology, Guangdong Provincial Key Laboratory of Major Obstetric Diseases, Guangdong Provincial Clinical Research Center for Obstetrics and Gynecology, Guangdong-Hong Kong-Macao Greater Bay Area Higher Education Joint Laboratory of Maternal-Fetal Medicine, The Third Affiliated Hospital, Guangzhou Medical University, Guangzhou, 510150, People’s Republic of China

*These authors contributed equally to this work

Correspondence: Qian Chen; Zhijian Wang, Department of Obstetrics and Gynecology, Nanfang Hospital, Southern Medical University, Guangzhou, 510515, People’s Republic of China, Email chenqianqian430@qq.com; wzjnfyy@163.com

Purpose: To elucidate the association between CD36 expression and senescence induced by oxidized low-density lipoprotein (ox-LDL) in patients with preeclampsia (PE).
Patients and Methods: We conducted a gene set enrichment analysis on RNA-sequencing data of placentas, focusing on CD36, a key gene in lipid metabolism. CD36 and ox-LDL expression were measured via qRT-PCR, Western blotting, immunohistochemistry, and immunofluorescence. We used plasmid and siRNA transfection to modulate CD36 expression in human umbilical vein endothelial cells, exposing them to ox-LDL to assess cellular senescence, oxidative stress, and angiogenesis. A co-culture system was constructed to examine how endothelial cell senescence affects trophoblast migration and invasion.
Results: In patients with PE, CD36 expression significantly increased in the vascular endothelial cells of the placenta. An association was observed between elevated CD36 and ox-LDL-induced cell senescence, accompanied by intracellular oxidative stress, endothelial cell angiogenesis disorders, and decreased trophoblast function in the placenta.
Conclusion: Our study has initially identified significant alterations in CD36 expression in PE placentas, which may be one of the driving factors for the occurrence of senescence. Further research is warranted to explore the mechanism between CD36 and PE-related placental senescence, which may offer novel avenues for the diagnosis and treatment of PE.

Keywords: placenta, preeclampsia, CD36, placental senescence, endothelial injury