ArticleAustin journal of vascular medicine2015
The Acute Respiratory Distress Syndrome: Mechanisms and Perspective Therapeutic Approaches.
Article in Austin journal of vascular medicine, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 103 papers, 1 of them a synthesis that pooled it.
What it found
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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
103 citing papers in PubMed, 1 synthesis or guideline pooled it, 142 citations in OpenAlex.
- Liver injury associated with the severity of COVID-19: A meta-analysis.Frontiers in public health · 2023Pooled it
- Efficacy of low-intensity pulsed ultrasound in the treatment of COVID-19 pneumonia.Ultraschall in der Medizin (Stuttgart, Germany : 1980) · 2023Trial
- Review
- Discovery of a novel cannabidiol-derived transient receptor potential vanilloid 4 inhibitor to reduce pulmonary edema and lung vascular permeability in mice.Cellular & molecular biology letters · 2026Article
- Early Antibiotic Discontinuation for Children With a Positive Rapid Respiratory Viral Test Hospitalized for Suspected Bacterial Tracheostomy-Associated Infections.Pediatric pulmonology · 2026Article
- Article
- Neutrophil-macrophage crosstalk network in acute lung injury: feedback circuits linking cytokine storm and cell death.Frontiers in cellular and infection microbiology · 2026Review
- Safety of a novel portable inhaled nitric oxide generator for therapy of persistent pulmonary hypertension in neonates: a case series study.Translational pediatrics · 2025Article
- Metabolic Interplay in Acute Lung Injury: PARK7 Integrates FADS1/2-Dependent PUFA Metabolism and H3K14 Lactylation to Attenuate Endothelial Ferroptosis and Dysfunction.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Post-burn Lung Inflammation Is Associated With Induction of Pulmonary Cathelicidin-related Antimicrobial Peptide and S100a8 in Mice.Journal of burn care & research : official publication of the American Burn Association · 2025Article
- Protective Effect of Low 2-O, 3-O Desulfated Heparin (ODSH) Against LPS-Induced Acute Lung Injury in Mice.Biomolecules · 2025Article
- Review
- Octreotide and direct/indirect lung injury.Research in pharmaceutical sciences · 2025Review
- Protective Effects of Pasireotide in LPS-Induced Acute Lung Injury.Pharmaceuticals (Basel, Switzerland) · 2025Article
- Therapeutic efficacy of deslanoside in oleic acid-induced acute lung injury in rabbits: Implications for clinical drug use and pharmacological strategies.Frontiers in pharmacology · 2025Article
- Endothelial ENaC as a repressor of oxidative stress and a guardian of lung capillary barrier function in bacterial and viral pneumonia.Frontiers in physiology · 2025Review
- Roles of oral anticoagulant use on the risk of 28-day mortality and in-hospital mortality in patients with acute respiratory distress syndrome.Frontiers in pharmacology · 2025Article
- Therapeutic characteristics of alveolar-like macrophages in mouse models of hyperoxia and LPS-induced lung inflammation.American journal of physiology. Lung cellular and molecular physiology · 2024Article
- PNSC928, a plant-derived compound, specifically disrupts CtBP2-p300 interaction and reduces inflammation in mice with acute respiratory distress syndrome.Biology direct · 2024Article
- Mechanisms of pulmonary endothelial barrier dysfunction in acute lung injury and acute respiratory distress syndrome.Chinese medical journal pulmonary and critical care medicine · 2024Article
43 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Acute Respiratory Distress Syndrome (ARDS) is a severe lung inflammatory disorder with a 30-50% mortality. Sepsis and pneumonia are the leading causes of ARDS. On the cellular level there is pulmonary capillary endothelial cell permeability and fluid leakage into the pulmonary parenchyma, followed by neutrophils, cytokines and an acute inflammatory response. When fluid increases in the interstitium then the outward movement continues and protein rich fluid floods the alveolar spaces through the tight junctions of the epithelial cells. Neutrophils play an important role in the development of pulmonary edema associated with acute lung injury or ARDS. Animal studies have shown that endothelial injury appears within minutes to hours after Acute Lung Injury (ALI) initiation with resulting intercellular gaps of the endothelial cells. The Endothelial Cell (EC) gaps allow for permeability of fluid, neutrophils and cytokines into the pulmonary parenchymal space. The neutrophils that infiltrate the lungs and migrate into the airways express pro-inflammatory cytokines such as tumor necrosis factor-alpha (TNF-α), interleukin-1 beta (IL-1β), and contribute to both the endothelial and epithelial integrity disruption of the barriers. Pharmacological treatments have been ineffective. The ARDS Network trial identified low tidal volume mechanical ventilation, positive end expiratory pressure and fluid management guidelines that have improved outcomes for patients with ARDS. Extracorporeal membrane oxygenation is used in specialized centers for severe cases. Prone positioning has recently proven to have significantly decreased ventilator days and days in the intensive care unit. Current investigation includes administration of mesenchymal stem cell therapy, partial fluid ventilation, TIP peptide nebulized administration and the continued examination of pharmacologic drugs.
Indexed as
Identifiers
26973981PMC4786180W2297960835What 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.