@article{Wu2026, 
author = {Chenggao Wu and Jiamei Hu and Wei Liu and Linju Kuang and Yize Wu and Aiping Le},
title = {Nanoscale platelet extracellular vesicles mediate inflammatory lung injury through Cd36–Fyn-dependent macrophage polarization in transfusion-related acute lung injury},
year = {2026},
journal = {Nano Research},
volume = {19},
number = {5},
pages = {94908388},
keywords = {transfusion-related acute lung injury, platelet-derived extracellular vesicles, M1 macrophages, Cd36–Fyn pathway, therapeutic strategy},
url = {https://www.sciopen.com/article/10.26599/NR.2026.94908388},
doi = {10.26599/NR.2026.94908388},
abstract = {Platelet-derived extracellular vesicles (pEVs) are abundant nanoscale bioeffectors released during platelet storage, yet their functional roles in transfusion-associated complications remain largely unexplored. The present study demonstrates that pEVs act as potent nanocarriers that aggravate transfusion-related acute lung injury (TRALI) through activation of the Cd36–Fyn signaling pathway in macrophages. Integrated single-cell RNA sequencing and mechanistic analyses demonstrated that pEVs administration selectively induced M1 macrophage polarization and amplified pulmonary inflammation. Cd36 was markedly upregulated in the Fn1+ macrophage subset, serving as the receptor that mediates pEV uptake and Fyn activation. Molecular and pharmacological inhibition of Cd36–Fyn signaling significantly attenuated pro-inflammatory cytokine expression, lung tissue damage, and mortality in vivo. These findings elucidate how nanoscale platelet vesicles reprogram macrophage responses and disrupt immune homeostasis, providing a mechanistic framework for understanding TRALI progression. Identification of the Cd36–Fyn axis as a molecular link between nanovesicle signaling and immune dysregulation highlights new therapeutic opportunities for transfusion safety and nanomedicine-based interventions.}
}