ArticleJournal of extracellular vesicles2024
Endothelial cell-derived extracellular vesicles expressing surface VCAM1 promote sepsis-related acute lung injury by targeting and reprogramming monocytes.
Article in Journal of extracellular vesicles, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
54 citing papers in PubMed, 58 citations in OpenAlex.
- Review
- The Acute Respiratory Distress Syndrome (ARDS): epidemiology, etiology, molecular mechanisms, diagnosis and therapeutic strategies.Molecular biomedicine · 2026Review
- Redirecting Monocyte Differentiation With Engineered Extracellular Vesicles for Glioma Immunotherapy.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- TRPV4/IP3R-1-mediated endothelial pyroptosis drives pulmonary microvascular endothelial permeability in endotoxin-induced acute lung injury.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026Article
- Multiple organ dysfunction syndrome: molecular mechanisms and therapeutic strategies.Signal transduction and targeted therapy · 2026Review
- Impact of altered HDL2b/HDL3 ratio on the function of innate immune cells in sepsis.Lipids in health and disease · 2026Article
- Macrophage PSRC1 attenuates atherosclerosis via extracellular vesicle-mediated MBD2 delivery to induce PCSK9 promoter methylation in hepatocytes.Cell & bioscience · 2026Article
- Bone Marrow Failure Model Mimics Aplastic Anemia Patients: Single-Cell Landscape of Immune Response Reveals Novel Mechanisms of Immune Imbalance in AA.Cancer medicine · 2026Article
- Decoding Immune Dysregulation in Sepsis Through Extracellular Vesicles: A Path to Precision Medicine.Pharmaceutics · 2026Review
- NsPEFs-enriched ADSCs-EVs alleviate osteoarthritis via RSPO3-mediated dual pro-chondrogenic and pro-M2 macrophage properties.Bioactive materials · 2026Article
- Association between the monocyte-to-lymphocyte ratio and 28-day all-cause mortality in sepsis-associated delirium patients: a retrospective study and machine learning.BMC infectious diseases · 2026Article
- Pulmonary Vascular Endothelial Cells in Lung Diseases: Mechanisms, Therapeutic Strategies, and Future Directions.Cell proliferation · 2026Review
- Endothelium-Treg Communication Through Extracellular Vesicle Transfer Exacerbates Acute Respiratory Distress Syndrome.Journal of extracellular vesicles · 2026Article
- Circ-PRKCI attenuates acute lung injury secondary to sepsis by targeting the miR-106b-5p/GAB1 axis.European journal of medical research · 2026Article
- The Application and Challenges of Stem Cell-Derived Extracellular Vesicles in Inhalation Lung Injury.International journal of nanomedicine · 2026Review
- Innate immune circuits in acute lung injury: macrophage plasticity, ILC crosstalk, and tissue repair failure.Frontiers in immunology · 2026Review
- Single-Cell and Spatial Transcriptomics Identify the Mono-S100A4 Subset Associated with Sepsis-Induced Lung Injury via the MIF-(CD74+CD44) Axis.Journal of inflammation research · 2026Article
- Mitochondrial dysfunction in sepsis-induced immunoparalysis: from immune-cell metabolic reprogramming to clinical biomarkers.Frontiers in immunology · 2026Review
- Source-renewing ectopic ApoB-TRL lipolysis in non-resolving ARDS: a testable spatial hypothesis.Frontiers in immunology · 2026Article
- Immune dysregulation inFrontiers in immunology · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
13 authors at 1 institution in 1 country.
Funding
Abstract
Acute lung injury (ALI)/acute respiratory distress syndrome (ARDS) is a common life-threatening syndrome with no effective pharmacotherapy. Sepsis-related ARDS is the main type of ARDS and is more fatal than other types. Extracellular vesicles (EVs) are considered novel mediators in the development of inflammatory diseases. Our previous research suggested that endothelial cell-derived EVs (EC-EVs) play a crucial role in ALI/ARDS development, but the mechanism remains largely unknown. Here, we demonstrated that the number of circulating EC-EVs was increased in sepsis, exacerbating lung injury by targeting monocytes and reprogramming them towards proinflammatory macrophages. Bioinformatics analysis and further mechanistic studies revealed that vascular cell adhesion molecule 1 (VCAM1), overexpressed on EC-EVs during sepsis, activated the NF-κB pathway by interacting with integrin subunit alpha 4 (ITGA4) on the monocyte surface, rather than the tissue resident macrophage surface, thereby regulating monocyte differentiation. This effect could be attenuated by decreasing VCAM1 levels in EC-EVs or blocking ITGA4 on monocytes. Furthermore, the number of VCAM1
Indexed as
Identifiers
What OpenQuestion holds
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 OpenQuestion graph.