ArticleJournal of inflammation research2025
Fatty Acid Transporter CD36 Promotes Ox-LDL-Induced Senescence of Vascular Endothelial Cells in Preeclampsia.
Article in Journal of inflammation research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
3 citing papers in PubMed.
- Investigation of oxidized low-density lipoprotein (oxLDL)-induced inflammation in atherosclerosis using a paper-based immune-vascular model.Analytical and bioanalytical chemistry · 2026Article
- CD36: bridging metabolism, inflammation, and reproduction.npj metabolic health and disease · 2026Review
- LDL oxidation and cerebrovascular aging: mechanisms of endothelial dysfunction, inflammation, and vascular cognitive impairment and dementia.Redox biology · 2026Review
Corrections and comments
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Authors and funding
18 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
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.
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