ReviewFrontiers in cell and developmental biology2025
Unraveling the deadly dance: endothelial cells and neutrophils in sepsis-induced acute lung injury/acute respiratory distress syndrome.
Review in Frontiers in cell and developmental biology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 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
17 citing papers in PubMed.
- Evaluating the prognostic value of admission IL-8 and sST2 as biomarkers of early myocardial injury in severe community-acquired pneumonia.Annals of medicine · 2026Article
- Integrated Transcriptomic and Proteomic Analysis of the Pathogenic Mechanisms ofAnimals : an open access journal from MDPI · 2026Article
- Mechanism of Action ofBiology · 2026Article
- Ferroptosis-Senescence Crosstalk in Sepsis-Associated Acute Lung Injury: Mechanisms and Therapeutic Opportunities.Biomedicines · 2026Review
- NETosis in the Kidney, Liver, and Lung of Mice With Cecal Ligation and Puncture-Induced Sepsis and the Ameliorating Effects of Adipose-Derived Stem Cell Exosomes.The Kaohsiung journal of medical sciences · 2026Article
- PRMT5 Mediates Sepsis-Associated Lung Injury by Modulating JAK1 Arginine Methylation: A Mechanism Study.The Kaohsiung journal of medical sciences · 2026Article
- Emerging biomodels to understand the pathophysiology of sepsis and evaluate new therapeutic strategies targeting extracellular histones.Materials today. Bio · 2026Review
- Progress on the mechanism of Piezo1 in mechanical ventilation-induced lung injury.Journal of thoracic disease · 2026Review
- Restrictive Versus Liberal Fluid Strategy for Initial Resuscitation in Sepsis and Septic Shock: A Systematic Review and Meta Analysis.Journal of clinical medicine research · 2026Article
- Dissecting Cell Death Pathways in Influenza A Virus Infection: Comparative Insights from Human Models.Viruses · 2026Review
- Curcumin Attenuates Lipopolysaccharide-Induced Acute Lung Injury Through Anti-Inflammatory Effects in RAW Cells.Chonnam medical journal · 2026Article
- Exploring the Mechanism of Bu Zhong Yi Qi Decoction in Treating Sepsis-induced Acute Lung Injury based on Network Pharmacology and Experimental Verification.Current pharmaceutical design · 2026Article
- Biomarkers for Pediatric Acute Respiratory Distress Syndrome: A Systematic Review.Journal of inflammation research · 2026Review
- One syndrome, many diseases: toward precision pharmacotherapy in acute respiratory distress syndrome.Frontiers in pharmacology · 2026Review
- Extracellular vesicles as emerging platforms for modulating innate immune responses in sepsis-associated acute lung injury.Frontiers in immunology · 2026Review
- Mechanosensitive channel Piezo1 in calcium dynamics: structure, function, and emerging therapeutic strategies.Frontiers in molecular biosciences · 2025Review
- Single-cell transcriptional profiling revealed the protective effects of Buddleoside in sepsis-associated acute liver injury.Frontiers in immunology · 2025Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Sepsis-induced acute lung injury (ALI) and acute respiratory distress syndrome (ARDS) are severe complications with high morbidity and mortality rates, characterized primarily by diffuse alveolar damage, endothelial dysfunction, and local inflammatory responses. Neutrophils and endothelial cells (ECs) play crucial roles in the pathogenesis and progression of these diseases. Neutrophils are important regulators of inflammation, while endothelial dysfunction exacerbates vascular permeability and the inflammatory cascade. The interaction between neutrophils and ECs is vital for the development of ALI/ARDS induced by sepsis, driving the pathological processes of inflammation and tissue damage. Despite advancements in treatment strategies such as protective mechanical ventilation and fluid management, effective methods for rapid lung tissue recovery or significant improvement in outcomes remain lacking. Therefore, we comprehensively summarize the current literature to gain deeper insights into the roles of neutrophils, ECs, and their interactions in sepsis-induced ALI/ARDS, hoping to provide critical insights into the mechanisms underlying sepsis-related ALI/ARDS and potential pathways for developing new therapeutic approaches.
Indexed as
Identifiers
What Socratic 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 Socratic graph.