ArticleJournal of cell science2023
Inflammatory macrophage to hepatocyte signals can be prevented by extracellular vesicle reprogramming.
Article in Journal of cell science, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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.
The trial behind it
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
7 citing papers in PubMed, 12 citations in OpenAlex.
- Iron-related intercellular communication in the liver: Main players and mechanisms.European journal of clinical investigation · 2026Review
- Integrated single-cell transcriptomics and proteomics elucidate the molecular mechanisms and detoxification strategy of rifampicin-induced hepatotoxicity.International journal of biological sciences · 2026Article
- RILP cleavage links an inflammatory state to enhanced tau propagation in a cell culture model of Alzheimer's disease.Molecular biology of the cell · 2025Article
- Extracellular vesicles in osteoarthritis: mechanisms, therapeutic potential, and diagnostic applications.Frontiers in immunology · 2025Review
- Editorial: Lipid metabolism in metabolic dysfunction- associated steatotic liver disease.Frontiers in medicine · 2025Article
- Extracellular Vesicles Modulate Liver Cells Viability and Reactive Oxygen Species in Patients Following a Very Low-Calorie Ketogenic Diet.Nutrients · 2024Article
- Unlocking the hepatoprotective potential of the parasitic plantFrontiers in pharmacology · 2023Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Macrophage-derived extracellular vesicles (EVs) play key roles in intercellular communication. Within the liver, they have been linked to several inflammatory diseases including nonalcoholic fatty liver disease (NAFLD). In this study, we found that inflammatory macrophages cause injury to hepatocytes, in part by a cell-cell crosstalk phenomenon involving the secretion of EVs containing pro-inflammatory cargo. Incorporation of these inflammatory signals into EV requires the cleavage of the trafficking adaptor protein RILP, which, as previously shown, results from inflammasome-mediated caspase-1 activation. RILP cleavage can be blocked by overexpressing a dominant negative, non-cleavable form of RILP (ncRILP). EV preparations from ncRILP-expressing cells are, by themselves, sufficient to suppress inflammatory effects in hepatocytes. These results suggest that both direct RILP manipulation and/or supplying ncRILP-modified EVs could be used as a novel therapy for the treatment of inflammatory liver diseases.
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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.