ArticleAmerican journal of respiratory cell and molecular biology2014
2-O, 3-O-desulfated heparin inhibits neutrophil elastase-induced HMGB-1 secretion and airway inflammation.
Article in American journal of respiratory cell and molecular biology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 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
33 citing papers in PubMed, 49 citations in OpenAlex.
- Emerging Role, Molecular Mechanisms, and Therapeutic Potential of 2-O, 3-O Desulfated Heparin (ODSH) Across Inflammatory and Vascular Diseases.Antioxidants (Basel, Switzerland) · 2026Review
- CX-01 mitigates trauma-induced acute kidney injury and improves survival in a combat-relevant polytrauma rat model.Frontiers in pharmacology · 2026Article
- Extracellular vesicle proteomics identify neutrophils as potential mediators of bladder radiotoxicity in prostate cancer.Cancer letters · 2025Article
- The Preventive and Therapeutic Effects of Acute and Severe Inflammatory Disorders with Heparin and Heparinoid.Biomolecules · 2024Review
- Diminished airway host innate response in people with cystic fibrosis who experience frequent pulmonary exacerbations.The European respiratory journal · 2024Article
- Homogeneous, Synthetic, Non-Saccharide Glycosaminoglycan Mimetics as Potent Inhibitors of Human Cathepsin G.Biomolecules · 2023Article
- Heparin, Low Molecular Weight Heparin, and Non-Anticoagulant Derivatives for the Treatment of Inflammatory Lung Disease.Pharmaceuticals (Basel, Switzerland) · 2023Review
- Article
- Neutrophil Elastase Triggers the Release of Macrophage Extracellular Traps: Relevance to Cystic Fibrosis.American journal of respiratory cell and molecular biology · 2022Article
- Neutrophil Elastase and Chronic Lung Disease.Biomolecules · 2021Review
- 2-O, 3-O desulfated heparin (ODSH) increases bacterial clearance and attenuates lung injury in cystic fibrosis by restoring HMGB1-compromised macrophage function.Molecular medicine (Cambridge, Mass.) · 2021Article
- Polysulfated Hyaluronan GlycoMira-1111 Inhibits Elastase and Improves Rheology in Cystic Fibrosis Sputum.American journal of respiratory cell and molecular biology · 2021Article
- Design and Rationale of a Randomized, Double-Blind, Placebo-Controlled, Phase 2/3 Study Evaluating Dociparstat in Acute Lung Injury Associated with Severe COVID-19.Advances in therapy · 2021Article
- Extracellular HMGB1: a therapeutic target in severe pulmonary inflammation including COVID-19?Molecular medicine (Cambridge, Mass.) · 2020Review
- Targeting Proteases in Cystic Fibrosis Lung Disease. Paradigms, Progress, and Potential.American journal of respiratory and critical care medicine · 2020Review
- Glycosaminoglycans as Multifunctional Anti-Elastase and Anti-Inflammatory Drugs in Cystic Fibrosis Lung Disease.Frontiers in pharmacology · 2020Review
- The Role of HMGB1, a Nuclear Damage-Associated Molecular Pattern Molecule, in the Pathogenesis of Lung Diseases.Antioxidants & redox signaling · 2019Review
- Glycosaminoglycans and Glycosaminoglycan Mimetics in Cancer and Inflammation.International journal of molecular sciences · 2019Review
- Leukocyte Heparanase: A Double-Edged Sword in Tumor Progression.Frontiers in oncology · 2019Review
- Role of using two-route ulinastatin injection to alleviate intestinal injury in septic rats.Chinese journal of traumatology = Zhonghua chuang shang za zhi · 2018Article
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
Abstract
Neutrophil elastase (NE) is a major inflammatory mediator in cystic fibrosis (CF) that is a robust predictor of lung disease progression. NE directly causes airway injury via protease activity, and propagates persistent neutrophilic inflammation by up-regulation of neutrophil chemokine expression. Despite its key role in the pathogenesis of CF lung disease, there are currently no effective antiprotease therapies available to patients with CF. Although heparin is an effective antiprotease and anti-inflammatory agent, its anticoagulant activity prohibits its use in CF, due to risk of pulmonary hemorrhage. In this report, we demonstrate the efficacy of a 2-O, 3-O-desulfated heparin (ODSH), a modified heparin with minimal anticoagulant activity, to inhibit NE activity and to block NE-induced airway inflammation. Using an established murine model of intratracheal NE-induced airway inflammation, we tested the efficacy of intratracheal ODSH to block NE-generated neutrophil chemoattractants and NE-triggered airway neutrophilic inflammation. ODSH inhibited NE-induced keratinocyte-derived chemoattractant and high-mobility group box 1 release in bronchoalveolar lavage. ODSH also blocked NE-stimulated high-mobility group box 1 release from murine macrophages in vitro, and inhibited NE activity in functional assays consistent with prior reports of antiprotease activity. In summary, this report suggests that ODSH is a promising antiprotease and anti-inflammatory agent that may be useful as an airway therapy in CF.
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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.