Burn-associated metabolic dysfunction: could extracellular vesicles play a role?
Farahat M., DadashiZadeh G., Ricciuti Z., Pappas A., Jeschke MG.
Narrative Review on Type 2 Diabetes, Burns, published in Clin Sci (Lond) (2026) — summary generated from the PubMed abstract.
Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.
- Level A · Stronger Clinical Evidence
- Level B · Emerging clinical evidence with positive signals
- Level C · Early human research exploring benefits
- Level D · Scientific groundwork from lab and animal studies
- Emerging · Emerging topic under active research
This page is generated from the PubMed record. The Thai description is an automated summary of bibliographic fields and the abstract, not a full translation, and is not medical advice.
- Study type
- Narrative Review
- Journal
- Clin Sci (Lond) (2026)
- Reported sample size
- —
- Source database
- Europe PMC
- PMID
- 41994933
- PMCID
- PMC13142934
- DOI
- 10.1042/cs20260147
Abstract (original English)
Hypermetabolism is a well-recognized component of the detrimental systemic response following severe burn injury. Despite extensive clinical observations and research output, the underlying mechanisms that drive this persistent metabolic dysregulation remain poorly understood. One emerging area of interest is the role of extracellular vesicles (EVs), small membrane-bound particles released by cells that are increasingly recognized as important mediators of intercellular communication and contributors to various pathological conditions. Recent studies have highlighted their significant involvement in metabolic regulation, acting as carriers of bioactive molecules that influence metabolic pathways in recipient cells. EVs contribute to the modulation of glucose and lipid metabolism, insulin sensitivity, mitochondrial function, and inflammation, thereby influencing systemic metabolic homeostasis. In this context, EVs have been proposed as potential mediators in the metabolic problems that follow severe burn injuries. Burn-induced hypermetabolism, marked by insulin resistance, muscle wasting, and systemic inflammation, is affected by exosome-driven signaling between damaged tissues and metabolic organs. Exosomes released after a burn carry inflammatory cytokines, stress-response proteins, and metabolic regulators that change cellular functions in distant organs such as the liver, sk
What this study does not prove
- • This study does not prove SVF is an approved treatment or a replacement for standard care.
- • This is a narrative review: it collects no new patient data and does not systematically appraise evidence quality.
Evidence level
Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.
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