Restorative endothelium and polarization-assisted inflammatory regulation nanomedicine (REPAIR) for acute lung injury treatment.
4 affiliations
- 1Department of Emergency, The Second Affiliated Hospital of Guangzhou Medical University, Guangzhou, 510260, PR China.
- 2Guangdong Provincial Key Laboratory of Molecular Target & Clinical Pharmacology, The NMPA and State Key Laboratory of Respiratory Disease, School of Pharmaceutical Sciences, Guangzhou Medical University, Guangzhou, 511436, PR China.
- 3School of Biomedical Engineering, Southern Medical University, Guangzhou, 510515, PR China.
- 4Department of Respiratory and Critical Care Medicine, The First People's Hospital of Foshan (Foshan Hospital Affiliated to Southern University of Science and Technology), School of Medicine, Southern University of Science and Technology, Foshan, 528000, PR China.
Abstract
Acute lung injury (ALI) is marked by uncontrolled inflammation and excessive immune cell infiltration, ultimately causing endothelial barrier disruption and impaired pulmonary function. To counteract these pathological processes, we develop a Restorative Endothelium and Polarization-Assisted Inflammatory Regulation nanomedicine (REPAIR) that integrates endothelial protection with alveolar macrophage reprogramming. REPAIR is fabricated by loading the P2X7 receptor (P2X7R) antagonist A740003 into apoptotic NIH3T3 cell vesicles (Apo-Vesicles), thereby combining apoptotic cell-derived "eat-me" signals with targeted inhibition of P2X7R-mediated inflammatory pathways. Benefiting from its apoptotic cell-mimetic surface, REPAIR exhibits markedly enhanced uptake by alveolar macrophages (AMs), driving the transition of pro-inflammatory M1 macrophages toward an anti-inflammatory M2 phenotype. At the same time, the released A740003 efficiently suppresses P2X7R activation, preventing macrophage necrosis and preserving endothelial vascular endothelial (VE)-cadherin to maintain vascular barrier integrity. In vitro and in vivo studies further confirm that REPAIR substantially reduces inflammatory cytokine production, limits macrophage necrosis, and stabilizes endothelial junctions through the synergistic interplay of apoptotic mimicry and P2X7R antagonism. These results highlight REPAIR as a promising and mechanistically comprehensive nanotherapeutic strategy for ALI and other inflammation-driven pulmonary diseases.
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BibTeX
@article{li2026restorative,
title = {{Restorative endothelium and polarization-assisted inflammatory regulation nanomedicine (REPAIR) for acute lung injury treatment.}},
author = {Jianqiao Li and Xiayun Chen and Lichong Lu and Zhuofeng Li and Ziqi Liang and Zhouchuan Shao and Xinxuan Li and Ying Chen and Mingyuan Fan and Wenyu Qiu and Zhijian Ye and Hong Cheng and Shiying Li and Xiaohui Chen},
journal = {Materials today. Bio},
year = {2026},
month = oct,
doi = {10.1016/j.mtbio.2026.103794},
url = {https://europepmc.org/article/MED/42999782},
note = {CC BY-NC},
}
RIS
TY - JOUR
TI - Restorative endothelium and polarization-assisted inflammatory regulation nanomedicine (REPAIR) for acute lung injury treatment.
AU - Jianqiao Li
AU - Xiayun Chen
AU - Lichong Lu
AU - Zhuofeng Li
AU - Ziqi Liang
AU - Zhouchuan Shao
AU - Xinxuan Li
AU - Ying Chen
AU - Mingyuan Fan
AU - Wenyu Qiu
AU - Zhijian Ye
AU - Hong Cheng
AU - Shiying Li
AU - Xiaohui Chen
PY - 2026
DA - 2026/10/29
JO - Materials today. Bio
DO - 10.1016/j.mtbio.2026.103794
UR - https://europepmc.org/article/MED/42999782
AB - Acute lung injury (ALI) is marked by uncontrolled inflammation and excessive immune cell infiltration, ultimately causing endothelial barrier disruption and impaired pulmonary function. To counteract these pathological processes, we develop a Restorative Endothelium and Polarization-Assisted Inflammatory Regulation nanomedicine (REPAIR) that integrates endothelial protection with alveolar macrophage reprogramming. REPAIR is fabricated by loading the P2X7 receptor (P2X7R) antagonist A740003 into apoptotic NIH3T3 cell vesicles (Apo-Vesicles), thereby combining apoptotic cell-derived "eat-me" signals with targeted inhibition of P2X7R-mediated inflammatory pathways. Benefiting from its apoptotic cell-mimetic surface, REPAIR exhibits markedly enhanced uptake by alveolar macrophages (AMs), driving the transition of pro-inflammatory M1 macrophages toward an anti-inflammatory M2 phenotype. At the same time, the released A740003 efficiently suppresses P2X7R activation, preventing macrophage necrosis and preserving endothelial vascular endothelial (VE)-cadherin to maintain vascular barrier integrity. In vitro and in vivo studies further confirm that REPAIR substantially reduces inflammatory cytokine production, limits macrophage necrosis, and stabilizes endothelial junctions through the synergistic interplay of apoptotic mimicry and P2X7R antagonism. These results highlight REPAIR as a promising and mechanistically comprehensive nanotherapeutic strategy for ALI and other inflammation-driven pulmonary diseases.
SN - 2590-0064
ER -