ArticleApplied biochemistry and biotechnology2026
Effects of Exercise on PVAT-Derived Exosomes in the Modulation of Vascular Function in Obese Mice.
Article in Applied biochemistry and biotechnology, 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
This study investigated whether perivascular adipose tissue (PVAT)-derived exosomal miRNAs contribute to exercise-induced improvement of vascular function in obesity. Male C57BL/6J mice were assigned to normal diet control (NC), high-fat diet control (HC), or high-fat diet with exercise (HE) groups. After 20 weeks of high-fat feeding, obese mice in the HE group underwent treadmill exercise for 8 weeks. Vascular contraction and relaxation were assessed in the presence or absence of PVAT-derived exosomes, which were further analyzed using a whole transcriptome sequencing. In vitro, vascular smooth muscle cells (VSMCs) were incubated with exosomes secreted from 3T3-L1 adipocytes (transfected with a miR-122-5p mimic) to evaluate phenotypic gene expression and migration. Compared with HC, arteries incubated with PVAT-conditioned medium from HE mice showed significantly reduced maximal constriction and improved endothelium-independent relaxation, whereas these effects were attenuated after removal of exosomes (P < 0.05). Exercise markedly altered the miRNA profile of PVAT-derived exosomes. Among these miRNAs, miR-122-5p was increased in obesity but decreased after exercise (P < 0.05). Exosomes enriched with miR-122-5p promoted VSMC migration and shifted phenotype gene expressions (down-regulated contractile ACTA2 and TAGLN and up-regulated synthetic SPP1; P < 0.05). This study is the first to show that PVAT-derived exosomes critically contribute to vascular function in obesity after exercise intervention. A unique exosomal miRNA signature may represent a potential regulatory mechanism underlying exercise-mediated vascular restoration, with miR-122-5p identified as a candidate molecule involved in triggering VSMC synthetic phenotype switching.
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