ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2026
Mesenchymal Stem Cell-Derived Extracellular Vesicles Modulate the Course of Peritoneal Inflammation Through Metabolic and Epigenetic Regulation.
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 3 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
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Who cites it
3 citing papers in PubMed.
- Innovative strategies for immune thrombocytopenia treatment: immunomodulatory mechanisms and clinical potential of mesenchymal stem cells.Stem cell research & therapy · 2026Review
- Mesenchymal stem cells and derived extracellular vesicles in major respiratory diseases: from multifaceted molecular mechanisms to clinical perspectives.Frontiers in cell and developmental biology · 2026Review
- Mesenchymal Stem Cell-Derived Extracellular Vesicles Modulate the Course of Peritoneal Inflammation Through Metabolic and Epigenetic Regulation.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
Corrections and comments
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Authors and funding
13 authors.
Funding
Abstract
Peritoneal dialysis (PD), as a renal replacement therapy, relies heavily on the structural and functional integrity of the peritoneum. In some patients, however, the peritoneum may undergo adverse remodeling and fibrotic thickening, resulting in treatment failure. Here, a previously unrecognized metabolic-epigenetic mechanism contributing to peritoneal fibrogenesis is uncovered, wherein lactate accumulation in injured peritoneal mesothelial cells promotes histone H3K18 lactylation and transcriptional activation of macrophage-recruiting chemokine CCL2. In a mouse model of peritoneal fibrosis induced by chlorhexidine gluconate (CG) or PD fluid, the administration of extracellular vesicles derived from human bone marrow mesenchymal stem cells (MSC-EVs) significantly ameliorates histological and functional changes in the peritoneum. Single-cell RNA sequencing reveals that MSC-EVs attenuate mesothelial-macrophage crosstalk by suppressing CCL2 signaling. Mechanistically, MSC-EVs reprogram glycolytic metabolism in mesothelial cells, reduce lactate production, and inhibit H3K18 lactylation-dependent transcriptional activation of CCL2. Pharmacologic blockade of lactate production recapitulates the protective effects of MSC-EVs. These findings suggest that lactate-induced histone lactylation is a key driver of peritoneal fibrosis, positioning MSC-EVs as a promising cell-free therapeutic strategy for targeting metabolic-epigenetic inflammation in serosal injury.
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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 Socratic graph.