Extracellular Vesicle-Mediated miR-155 from Visceral Adipocytes Induces Skeletal Muscle Dysplasia in Obesity

Quick Facts

  • Publication title: Extracellular Vesicle-Mediated miR-155 from Visceral Adipocytes Induces Skeletal Muscle Dysplasia in Obesity
  • Journal: cells
  • Year: 2025
  • DOI: 10.3390/cells14171302
  • PMID/PMCID: 40940715; PMC12427855

Research overview

Obesity poses a serious threat to human health, with induced skeletal muscle dysfunction significantly increasing the risk of metabolic syndrome. These findings provide novel mechanistic insights into obesity-induced skeletal muscle dysregulation and facilitate potential therapeutic strategies targeting exosomal miRNA signaling.

Key findings

Obesity poses a serious threat to human health, with induced skeletal muscle dysfunction significantly increasing the risk of metabolic syndrome.

In obesity, it is known that visceral adipose tissue (VAT) mediates the dysregulation of the adipose-muscle axis through exosome-delivered miRNAs, but the associated regulatory mechanisms remain incompletely elucidated.

7 cells/C2C12 cells) to demonstrate that high-fat diet-induced VA-derived extracellular vesicles (HFD VAD-evs) preferentially accumulate in skeletal muscle and induce developmental impairment.

HFD VAD-evs disrupt skeletal muscle homeostasis through dual mechanisms: the direct suppression of myoblast development via exosomal miR-155 cargo and the indirect inhibition of myogenesis through macrophage-mediated inflammatory responses in skeletal muscle.

Echo Biotech Role

Echo Biotech contributed cargo loading; the study also used or cited ExoLoad®.

Related platforms: Echosome®, Research Reagents & Tools

Related services and capabilities: Small RNA / Cargo Loading, Research Reagent / Product Supply

Related products or reagents: ExoLoad® Nucleic Acid Loading Kit

References

Original publication: Extracellular Vesicle-Mediated miR-155 from Visceral Adipocytes Induces Skeletal Muscle Dysplasia in Obesity cells. 2025. DOI: 10.3390/cells14171302. PMID/PMCID: 40940715; PMC12427855.