Level D· Scientific groundwork from lab and animal studiesLaboratory StudyPubMed

Engineered Young Brown Adipose Tissue-Derived Exosomes Alleviate Radiation-Induced Lung Injury by Promoting G Protein-Coupled Receptor 183 Ubiquitination.

Guan H., Yang J., Han Y., Pan H., Luo J., Wang Y.

Laboratory Study on Chronic Inflammation, published in ACS Nano (2026) — summary generated from the PubMed abstract.

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Level D· Scientific groundwork from lab and animal studiesEvidence level of this study

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
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Study type
Laboratory Study
Journal
ACS Nano (2026)
Country
United States
Reported sample size
—
Source database
PubMed
PMID
42390833
DOI
10.1021/acsnano.6c05744

Abstract (original English)

Acute radiation-induced lung injury is a serious and potentially life-threatening complication of radiotherapy for thoracic malignancies or accidental radiation exposure, characterized by high incidence, limited treatment options, and substantial mortality. To address the lack of effective therapies for preventing and treating radiation-induced lung injury, we developed an engineered nanoplatform, BAT-exo@Au, generated by functionalizing exosomes derived from young brown adipose tissue (BAT) with 1,2-distearoyl- sn -glycero-3-phosphoethanolamine-polyethylene glycol-thiol (DSPE-PEG-SH) and gold nanoparticles via chloroauric acid (HAuCl 4 ) incubation. Our results show that BAT-exo@Au was efficiently internalized by irradiated lung tissue and exerted radioprotective effects by suppressing reactive oxygen species production and attenuating radiation-induced inflammatory responses. In addition, BAT-exo@Au mitigated radiation-induced epithelial-mesenchymal transition while enhancing tumor radiosensitivity, suggesting a dual therapeutic advantage. Mechanistically, BAT-exo@Au reduced apoptosis and preserved mitochondrial membrane potential after radiation in vitro. Transcriptomic analysis identified G protein-coupled receptor 183 ( Gpr183 ) as a potential downstream target, showing upregulation after radiation but downregulation following BAT-exo@Au treatment. Further in vitro experim

What this study does not prove

  • • This study does not prove SVF is an approved treatment or a replacement for standard care.
  • • This is preclinical work; animal or laboratory results cannot be applied to humans.

Evidence level

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

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