Mesenchymal Stem Cell-Derived Extracellular Vesicles Modulate the Course of Peritoneal Inflammation through Metabolic and Epigenetic Regulation

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Mesenchymal Stem Cell-Derived Extracellular Vesicles Modulate the Course of Peritoneal Inflammation through Metabolic and Epigenetic Regulation

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Co-author 1

Qiang Huang huangq278@mail.sysu.edu.cn the Third Affiliated Hospital of Sun Yat-sen University Nephrology Division Guang zhou China -

Co-author 2

Hui Peng pengh@mail.sysu.edu.cn the Third Affiliated Hospital of Sun Yat-sen University Nephrology Division Guang zhou China *

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Introduction

Peritoneal dialysis (PD) efficacy depends on peritoneal integrity, which can be compromised by fibrotic thickening. This study investigates a novel metabolic-epigenetic pathway in peritoneal fibrogenesis, focusing on histone lactylation-driven chemokine activation.

Methods

Chlorhexidine gluconate (CG) or PD solution-induced peritoneal fibrosis mouse model was treated with mesenchymal stem cell-derived extracellular vesicles (MSC-EVs). Single-cell RNA sequencing (scRNA-seq) was performed on peritoneal tissues to analyze cellular interactions. Metabolic reprogramming in injured mesothelial cells was assessed via glycolysis and lactate production assays. Pharmacological inhibition of lactate production was used to validate the role of metabolic regulation. Mechanistic insights into epigenetic modulation were explored through CUT&Tag sequencing using an anti-H3K18la antibody.

Results

MSC-EV treatment significantly ameliorated peritoneal fibrosis and dysfunction. Single-cell analysis revealed attenuated mesothelial-macrophage crosstalk via suppression of CCL2 signaling. Mechanistically, MSC-EVs reprogrammed glycolytic metabolism in mesothelial cells, reducing lactate production and subsequent histone H3K18 lactylation, thereby inhibiting CCL2 transcription. Pharmacologic inhibition of lactate production mirrored these protective effects.

Conclusion

Lactate-induced H3K18 lactylation is a key driver of peritoneal fibrosis. MSC-EVs represent a promising cell-free therapy by targeting metabolic-epigenetic inflammation, offering a potential strategy for preserving peritoneal membrane function in PD.

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