ArticleJournal of nanobiotechnology2026
Endothelial-targeted modification of ginseng-derived exosomes for IL-6 SiRNA delivery ameliorates hepatic ischemia-reperfusion injury.
Article in Journal of nanobiotechnology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers, 1 of them a synthesis that pooled 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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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
3 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Exosomes orchestrate immune homeostasis in acute ischemia-reperfusion flap injury and chronic wounds: the TLR4/NF-κB-STAT3 R-ratio balance decision model, engineering optimization and translational clinical strategy.Frontiers in immunology · 2026Pooled it
- Advances in Research onInternational journal of molecular sciences · 2026Review
- Transcriptome-Based Dissection of the Molecular Mechanisms Underlying Flooding Stress Responses of Eastern Cottonwood in the Floodplains of the Middle and Lower Reaches of the Yangtze River.Plants (Basel, Switzerland) · 2026Article
Corrections and comments
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Authors and funding
17 authors.
Funding
Abstract
Liver ischemia-reperfusion injury (IRI) serves as a critical pathological basis for post-hepatectomy liver failure and graft dysfunction following liver transplantation. Excessive inflammatory responses, oxidative stress, and cell death are key mechanisms underlying IRI. The lack of multi-targeted therapies contributes to the current insufficiency in clinical IRI management. This study developed endothelial-targeting VHPKQHR peptide (VHP)-modified ginseng-derived exosomes (G-Exos) loaded with IL-6 small interfering RNA (Si-IL6) (siRNA@VG-Exos) to mitigate liver IRI. VHP modification facilitated the targeted delivery of siRNA@VG-Exos to damaged endothelium, promoting their accumulation and subsequent release at the IRI site. siRNA@VG-Exos effectively reduced hepatic inflammatory cytokine release, enhanced T-SOD and CAT expression while suppressing MDA generation, thereby alleviating oxidative stress. Furthermore, they promoted the restoration of mitochondrial membrane potential, maintaining mitochondrial homeostasis. Si-IL6 additionally suppressed IL-6 expression in liver tissue, synergistically enhancing the anti-inflammatory effect of G-Exos. Moreover, siRNA@VG-Exos inhibited CD86 expression and promoted CD206 expression in hepatic macrophages, facilitating their polarization from the pro-inflammatory M1 phenotype to the anti-inflammatory M2 phenotype and modulating immunity. Ultimately, siRNA@VG-Exos reduced hepatic necrotic areas, lowered ALT and AST levels, and restored liver tissue function. Further sequencing analysis indicated that siRNA@VG-Exos alleviates liver IRI by inhibiting immune and inflammatory responses and oxidative stress damage. Therefore, siRNA@VG-Exos provides a novel targeted strategy for the treatment of liver IRI.
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Registered trials
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.