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Characterization of Adipocyte-Derived Extracellular Vesicle Secretion Using a CD63-GFP Reporter Mouse Model In Vivo and In Vitro
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Extracellular Vesicles in Obesity: From Pathophysiological Mediators to Therapeutic Tools
Nikola Pavlović1,2, Petar Todorović3, Mirko Maglica4,5
1Department of Pathophysiology, University of Split School of Medicine, 21000 Split, Croatia.
International Journal of Molecular Sciences
|April 14, 2026
Summary
Obesity involves faulty cell communication via extracellular vesicles (EVs). These EVs spread metabolic dysfunction, but engineered EVs show promise for diagnosis and treatment in precision obesity medicine.
Area of Science:
- Cell biology
- Metabolic disease research
- Nanomedicine
Background:
- Obesity is increasingly viewed as a disease of dysregulated intercellular communication, mediated by extracellular vesicles (EVs).
- These nanoparticles, released by various cells, carry altered cargo in obesity, contributing to systemic metabolic dysfunction.
- Dysfunctional cells in obesity secrete EVs that propagate inflammation and insulin resistance.
Purpose of the Study:
- To explore the role of extracellular vesicles (EVs) in obesity pathogenesis and their potential as diagnostic biomarkers and therapeutic agents.
- To investigate how EVs mediate crosstalk between adipocytes, macrophages, and other cells in the context of obesity.
- To assess the therapeutic potential of engineered EVs for treating obesity-related metabolic disorders.
Main Methods:
- Analysis of EV cargo (miRNAs, lipids, proteins) from obese subjects.
- Preclinical studies using EVs to model and treat obesity-related conditions like insulin resistance and hepatic steatosis.
- Evaluation of engineered EVs and mesenchymal stem cell-derived EVs (MSC-EVs) in preclinical models.
- Review of early-phase clinical trials for EV-based therapies.
Main Results:
- Obesity is characterized by EVs carrying pro-inflammatory miRNAs and lipids, impairing metabolic functions.
- EVs from adipose tissue promote hepatic steatosis, insulin resistance, and endothelial dysfunction.
- EV-mediated crosstalk exacerbates adipose tissue inflammation.
- Circulating EVs serve as biomarkers for disease severity and cardiovascular risk.
- Therapeutic EVs, particularly MSC-EVs, show potential in reversing obesity-related pathologies in preclinical studies.
- Phase I trials indicate safety for MSC-EVs, but manufacturing challenges persist.
Conclusions:
- Extracellular vesicles are key mediators of obesity's complex intercellular communication, driving metabolic dysfunction.
- Circulating EVs offer valuable diagnostic and prognostic biomarkers for obesity and related cardiovascular risks.
- Engineered EVs represent promising therapeutic vehicles for precision obesity medicine, with early safety data available.
- Despite therapeutic potential, manufacturing scalability and cost remain significant barriers to clinical adoption.
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