ArticleClinical and experimental medicine2026
Adipose-derived mesenchymal stem cell-derived extracellular vesicles reduce glycolysis and polarize macrophages toward M2 phenotype in sepsis-associated acute kidney injury via the miR-574-5p/GLUT1 axis.
Article in Clinical and experimental medicine, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Extracellular vesicles (EVs) from adipose-derived mesenchymal stem cells (ADSCs) may exert a therapeutic benefit in sepsis-associated organ dysfunction by delivering cargos to target cells. The aims of this study were to explore the therapeutic efficacy and potential mechanism of microRNA (miR)-574-5p delivered by ADSC-EVs in sepsis-associated acute kidney injury (SA-AKI). EVs were isolated from mouse ADSCs and characterized by multilineage differentiation potency, morphology, and surface markers. miR-574-5p expression in ADSC-EVs was analyzed by biochemical testing. Luciferase reporter and RNA pull-down assays were employed to identify the binding relation between miR-574-5p and glucose transporter 1 (GLUT1). Cecal ligation and puncture (CLP)-induced mouse SA-AKI model administered with ADSC-EVs was used to evaluate therapeutic effects on kidney injury. ADSC-EVs were co-cultured with RAW264.7 macrophages to assess effects on inflammation, glycolysis (lactate levels, extracellular acidification rate), and macrophage polarization. ADSC-EVs elevated miR-574-5p expression and polarized macrophages toward M2 phenotype, reducing kidney dysfunction and inflammatory response in CLP mice. In vitro, ADSC-EVs arrested lipopolysaccharide-induced M1 macrophage polarization and induced M2 macrophage polarization by upregulating miR-574-5p expression. Mechanistically, ADSC-EVs transferred miR-574-5p into macrophages, where miR-574-5p targeted GLUT1 and limited its expression. This effect contributed to the inhibition of glycolysis and promotion of M2 macrophage polarization. In vivo studies confirmed these positive effects of ADSC-EVs in SA-AKI via the miR-574-5p/GLUT1 pathway. Altogether, our findings suggest that ADSC-EVs carrying miR-574-5p target GLUT1 to restrain glycolysis and prime M2 macrophage polarization in a SA-AKI model, paving the way for establishing a therapeutic approach for SA-AKI.
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