Evidence map›Paper›PMID 41866647›Full record

ArticleApoptosis : an international journal on programmed cell death2026

Targeted delivery of RGD-JEG-3-EVs for placental vascular regeneration in preeclampsia: from molecular mechanism toward therapy.

Qi Wang, Quanbo Liu, Xi Yuan

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Article in Apoptosis : an international journal on programmed cell death, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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1 · What the graph read from it

What it found

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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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3 · Its place in the literature

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4 · The record

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5 · Who and what money

Authors and funding

3 authors.

Qi WangDepartment of Obstetrics, Xiangya Hospital, Central South University, Changsha, 410008, Hunan, China.
Quanbo LiuDepartment of Spine Surgery, The First Affiliated Hospital, Hengyang Medical School, University of South China, Hengyang, 421001, Hunan, China.
Xi YuanDepartment of Blood Transfusion, Xiangya Hospital, Central South University, Xiangya Road 87, Changsha, 410008, Hunan, China. 690061719@qq.com.

Funding

General Project of the Health Commission of Hunan Province B202305026242Key Special Project of National Clinical Key Specialties of the Health Commission of Hunan Province Z2023015National Natural Science Foundation of China 82101789Natural Science Foundation of Hunan Province 2024JJ5551
6 · The paper itself

Abstract

Preeclampsia (PE) is a hypertensive disorder of pregnancy associated with placental dysfunction and vascular maladaptation. Defective remodeling of maternal spiral arteries leads to placental ischemia, a key driver of the maternal systemic syndrome. Extracellular vesicles (EVs) from highly invasive choriocarcinoma trophoblasts, which exhibit pro-angiogenic properties, represent a potential therapeutic resource. However, their utility for targeted therapy in PE remains unexplored. We engineered EVs derived from RGD-JEG-3-EVs on activated vasculature. The therapeutic potential and safety were evaluated in the L-NAME-induced rat model of gestational hypertension and endothelial dysfunction. A combination of in vivo imaging, functional assays in HUVECs, proteomic analysis, and molecular interventions was used to assess efficacy and mechanism. RGD-JEG-3-EVs exhibited preferential placental accumulation, alleviated maternal hypertension and proteinuria, improved fetal growth, and enhanced placental vascular density this model. Short-term tumorigenicity and toxicity assessments revealed no detectable adverse effects under experimental conditions. Proteomic profiling identified FASCIN as a key protein enriched in JEG-3-EVs. Functional studies indicated that FASCIN contributed to EV-mediated pro-angiogenic effects in a Wnt/β-catenin-dependent manner. Suppression of FASCIN attenuated the therapeutic benefits in vivo. This study provides proof-of-concept for using engineered RGD-JEG-3-EVs as a targeted strategy to deliver pro-angiogenic signals (FASCIN-Wnt/β-catenin signal) and improve placental vascular function in a rat model of gestational hypertension, supporting further investigation of this nanotherapeutic strategy.

Indexed as

Extracellular VesiclesOligopeptidesPlacentaPre-EclampsiaRegenerationAnimalsFemaleHumansHuman Umbilical Vein Endothelial CellsNeovascularization, PhysiologicPregnancyRatsRats, Sprague-DawleyTrophoblastsarginyl-glycyl-aspartic acidOligopeptidesAngiogenesisExtracellular vesiclesFASCINJEG-3 cellPreeclampsiaRGD peptide

Identifiers

PMID41866647

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.