ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2025
tRF-5004b Enriched Secretory Autophagosomes Induce Endothelial Cell Activation to Drive Acute Respiratory Distress Syndrome.
Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
4 citing papers in PubMed.
- The Acute Respiratory Distress Syndrome (ARDS): epidemiology, etiology, molecular mechanisms, diagnosis and therapeutic strategies.Molecular biomedicine · 2026Review
- Cardiovascular sequelae of Long COVID: immune dysregulation inflammation as central drivers.Frontiers in immunology · 2026Review
- tRF-5004b Enriched Secretory Autophagosomes Induce Endothelial Cell Activation to Drive Acute Respiratory Distress Syndrome.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Single-Cell Sequencing Redefines Immune Heterogeneity and Communication Networks in ARDS: Toward Precision Therapeutics.International journal of genomics · 2025Review
Corrections and comments
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Authors and funding
18 authors.
Funding
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 endothelial activation. Mechanically, tRF-5004b directly interacts with the nuclear transporter KPNA2, thereby facilitating the association between KPNA2 and the transcription factor p65. This interaction enhances p65 nuclear translocation, a process implicated in EC activation. Additionally, the level of tRF-5004b is positively correlated with the severity of ARDS, and patients with high tRF-5004b levels have a poor prognosis. Overall, it is found that tRF-5004b-enriched SAPs induce acute lung injury by promoting p65 nuclear translocation to activate ECs, suggesting that tRF-5004b may be a novel therapeutic target for ARDS.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.