ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2026
RPS3-Enriched Extracellular Vesicles Mediate Liver-Spinal Cord Inter-Organ Communication.
Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
2 citing papers in PubMed.
- Exosomes target liver TREM-1 to break the systemic inflammatory cascade and improve spinal cord injury outcomes.Journal of orthopaedic translation · 2026Article
- Transcriptomics Insights into Spinal Cord Injury for Therapy Development.International journal of molecular sciences · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
12 authors.
Funding
Abstract
Spinal cord injury (SCI) induces bidirectional inter-organ communication via extracellular vesicles (EVs) with multiple peripheral organs. Here, we identify the liver as a critical regulator that inhibits endogenous neuronal repair. Proteomics of plasma EVs from SCI patients and RNA-sequence of post-injury livers revealed a rapid increase of ribosomal protein S3 (RPS3) in plasma EVs and liver-derived EVs (LEVs). These RPS3-enriched LEVs are transported to the spinal cord lesion sites, where they are taken up by neural stem cells (NSCs) and astrocytes. Mechanistically, RPS3 activates nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) signaling in recipient cells, inhibiting NSC differentiation into neurons and oligodendrocytes and polarizing astrocytes toward a neuroinflammatory phenotype. Further detection identified activated Kupffer cells (KCs) as the primary source of RPS3, initiating an intra-hepatic cascade that further amplified RPS3 expression in hepatocytes. Crucially, in vivo depletion of KCs or hepatic RPS3 effectively attenuated NF-κB activation, restored axonal regeneration and remyelination, and promoted neurological functional recovery. This work highlights a liver-spinal cord axis wherein RPS3-enriched hepatic KC-derived EVs impair central nervous system (CNS) regeneration via the NF-κB activation, presenting a promising prognostic biomarker and novel therapeutic target for SCI.
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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.