TRF-5004b Enriched Secretory Autophagosomes Induce Endothelial Cell Activation to Drive Acute Respiratory Distress Syndrome.

ABSTRACT: Acute respiratory distress syndrome (ARDS) is an acute inflammatory lung injury for which effective therapeutic agents are lacking. Excessive endothelial cell (EC) activation is a critical trigger of inflammation. Extracellular vesicles (EVs) are increasingly recognized as prominent regulators of inflammatory responses. The previous study identified secretory autophagosomes (SAPs), a novel class of EVs, as a prognostic marker in ARDS, raising questions of whether and how they are involved in the pathogenesis of ARDS. Here, it is shown that inflamed macrophage-derived SAPs (MSAPs) exacerbate lung injury by weakening the role of ECs as gatekeepers of immune cell transport within the lung. Bioinformatics and functional studies reveal that tRF-5004b is a key molecule of MSAPs in mediating endo

SUBMITTER: Zhu XX 

PROVIDER: S-EPMC12412491 | biostudies-literature | 2025 Sep

REPOSITORIES: biostudies-literature