ArticleShock (Augusta, Ga.)2016
BLOCKADE OF ENDOTHELIAL GROWTH FACTOR, ANGIOPOIETIN-2, REDUCES INDICES OF ARDS AND MORTALITY IN MICE RESULTING FROM THE DUAL-INSULTS OF HEMORRHAGIC SHOCK AND SEPSIS.
Article in Shock (Augusta, Ga.), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers, 1 of them a synthesis that pooled it.
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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
19 citing papers in PubMed, 1 synthesis or guideline pooled it, 31 citations in OpenAlex.
- Circulating angiopoietin-2 and the risk of mortality in patients with acute respiratory distress syndrome: a systematic review and meta-analysis of 10 prospective cohort studies.Therapeutic advances in respiratory diseasePooled it
- Review
- Endothelial cell, but not neutrophil, programmed cell death receptor-ligand 1 loss has a morbid impact on experimental murine shock/sepsis-induced lung injury.Frontiers in immunology · 2026Article
- Role of Tie-2 Axis in Sepsis: A Potential Therapeutic Target.Journal of cellular and molecular medicine · 2025Review
- Mechanisms of immune suppression in sepsis/shock: one investigator's/lab group's experience (SLB 2024 legacy award presentation).Journal of leukocyte biology · 2025Article
- Combination of Physicochemical Tropism and Affinity Moiety Targeting of Lipid Nanoparticles Enhances Organ Targeting.Nano letters · 2024Article
- Editorial: Reviews in pulmonary medicine 2022.Frontiers in medicine · 2023Article
- Sulfasalazine prevents lung injury due to intra-abdominal sepsis in rats: possible role of Nrf2 and angiopoietin-2.Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica · 2023Article
- Efficacy and Safety of LY3127804, an Anti-Angiopoietin-2 Antibody, in a Randomized, Double-Blind, Placebo-Controlled Clinical Trial in Patients Hospitalized with Pneumonia and Presumed or Confirmed COVID-19.Clinical medicine insights. Circulatory, respiratory and pulmonary medicine · 2022Article
- Delayed angiopoietin-2 blockade reduces influenza-induced lung injury and improves survival in mice.Physiological reports · 2021Article
- Dynamic angiopoietin-2 assessment predicts survival and chronic course in hospitalized patients with COVID-19.Blood advances · 2021Article
- Endothelial Damage in Acute Respiratory Distress Syndrome.International journal of molecular sciences · 2020Review
- Blockade of endothelial, but not epithelial, cell expression of PD-L1 following severe shock attenuates the development of indirect acute lung injury in mice.American journal of physiology. Lung cellular and molecular physiology · 2020Article
- Alternative RNA splicing and alternative transcription start/end in acute respiratory distress syndrome.Intensive care medicine · 2020Article
- Review
- Short-term curative effect and safety of propranolol combined with laser in the treatment of infantile hemangiomas.Oncology letters · 2018Article
- PAD4 Deficiency Leads to Decreased Organ Dysfunction and Improved Survival in a Dual Insult Model of Hemorrhagic Shock and Sepsis.Journal of immunology (Baltimore, Md. : 1950) · 2018Article
- A novel role for coinhibitory receptors/checkpoint proteins in the immunopathology of sepsis.Journal of leukocyte biology · 2018Review
- Novel Role for PD-1:PD-L1 as Mediator of Pulmonary Vascular Endothelial Cell Functions in Pathogenesis of Indirect ARDS in Mice.Frontiers in immunology · 2018Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
We have demonstrated hemorrhagic shock "priming" for the development of indirect acute respiratory distress syndrome (iARDS) in mice following subsequent septic challenge, and show pathology characteristic of patients with iARDS, including increased lung microvascular permeability and arterial PO2/FI02 reduced to levels comparable to mild/moderate ARDS during the 48 h following hemorrhage. Loss of endothelial cell (EC) barrier function is a major component in the development of iARDS. EC growth factors, Angiopoietin (Ang)-1 and 2, maintain vascular homeostasis via tightly regulated competitive interaction with tyrosine kinase receptor, Tie2, expressed on ECs. Ang-2/Tie2 binding, in contrast to Ang-1, is believed to produce vessel destabilization, pulmonary leakage, and inflammation. Recent clinical findings from our trauma/surgical intensive care units and others have reported elevated Ang-2 in the plasma from patients that develop ARDS. We have previously described similarly elevated Ang-2 in plasma and lung tissue in our shock/sepsis model for the development of iARDS, and demonstrated effective reduction in indices of inflammation and lung tissue injury following siRNA inhibition of Ang-2 protein synthesis. In this study we show that Ang-2 in lung tissue and plasma spikes following hemorrhage (priming) and remain elevated at sepsis induction. In addition, that transient inhibition of Ang-2 function immediately following hemorrhage, suppressing priming, but not following sepsis, impacts the development of iARDS in our model. Our data demonstrate that selective temporal blockade of Ang-2 function following hemorrhagic shock priming significantly improved PO2/FIO2, decreased lung protein leak and indices of inflammation, and improved 10-day survival in our murine model for the development iARDS.
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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 OpenQuestion graph.