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Engineered Young Brown Adipose Tissue-Derived Exosomes Alleviate Radiation-Induced Lung Injury by Promoting G
Hua Guan1, Jingjing Yang2, Yang Han1
1Department of Radiation Biology, Beijing Key Laboratory for Radiobiology, Beijing Institute of Radiation Medicine, Beijing 100850, China.
ACS Nano
|July 2, 2026
Summary
Engineered exosomes from young brown adipose tissue (BAT), termed BAT-exo@Au, protect against radiation-induced lung injury by reducing inflammation and oxidative stress. This nanoplatform shows dual therapeutic potential, mitigating lung damage and enhancing tumor radiosensitivity.
Area of Science:
- Biomedical Engineering
- Nanotechnology
- Radiology
Background:
- Acute radiation-induced lung injury is a severe complication of radiotherapy with limited treatment options.
- Developing effective radioprotective strategies is crucial for improving patient outcomes.
Purpose of the Study:
- To develop and evaluate an engineered nanoplatform, BAT-exo@Au, for preventing and treating radiation-induced lung injury.
- To investigate the therapeutic mechanisms and dual advantages of BAT-exo@Au in mitigating lung damage and enhancing tumor radiosensitivity.
Main Methods:
- Functionalization of exosomes from young brown adipose tissue (BAT) with DSPE-PEG-SH and gold nanoparticles to create BAT-exo@Au.
- In vitro and in vivo assessment of BAT-exo@Au's radioprotective effects, including suppression of reactive oxygen species and inflammation.
- Evaluation of BAT-exo@Au's impact on epithelial-mesenchymal transition, tumor radiosensitivity, apoptosis, and mitochondrial membrane potential.
- Transcriptomic analysis to identify downstream targets, followed by in vitro validation of G protein-coupled receptor 183 (Gpr183) and NEDD4 interaction.
Main Results:
- BAT-exo@Au was efficiently internalized by irradiated lung tissue, demonstrating significant radioprotective effects.
- The nanoplatform suppressed reactive oxygen species, attenuated inflammation, and mitigated radiation-induced epithelial-mesenchymal transition.
- BAT-exo@Au reduced apoptosis, preserved mitochondrial membrane potential, and enhanced tumor radiosensitivity.
- Mechanism revealed that BAT-exo@Au downregulates Gpr183 by promoting its ubiquitination and degradation via interaction with NEDD4.
Conclusions:
- BAT-exo@Au shows promise as a preventive agent for radiation-induced lung injury.
- The nanoplatform offers a dual therapeutic advantage by protecting normal lung tissue and enhancing tumor radiosensitivity.
- Modulation of Gpr183 through enhanced Gpr183-NEDD4 interaction and ubiquitination is a key mechanism underlying BAT-exo@Au's efficacy.
