ArticleMolecular medicine (Cambridge, Mass.)2020
The α7 nicotinic acetylcholine receptor agonist, GTS-21, attenuates hyperoxia-induced acute inflammatory lung injury by alleviating the accumulation of HMGB1 in the airways and the circulation.
Article in Molecular medicine (Cambridge, Mass.), 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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Who cites it
30 citing papers in PubMed, 44 citations in OpenAlex.
- Dynamic Changes in Serum Choline Acetyltransferase and Acetylcholinesterase in Septic versus Non-Septic ICU Patients: A Prospective Exploratory Study.Journal of inflammation research · 2026Trial
- GTS-21 Alleviates Acute Lung Injury by Enhancing GLP-1 Secretion and Regulating Alveolar Surfactant Proteins via α7nAChR Activation.Inflammation · 2026Article
- Alpha-7 nicotinic acetylcholine receptor: targeting the interplay between inflammation, renin-angiotensin aldosterone system, and nervous system for the novel treatment of heart failure.Frontiers in pharmacology · 2026Review
- Advances in research on hyperoxia-induced acute lung injury: from pathogenesis to therapy.Frontiers in cell and developmental biology · 2026Review
- Nociceptor α7nAChR activation blunts neuronal HMGB1 release and attenuates inflammation and nociceptive behavior.Molecular medicine (Cambridge, Mass.) · 2025Article
- The cholinergic drug galantamine ameliorates acute and subacute peripheral and brain manifestations of acute respiratory distress syndrome in mice.Scientific reports · 2025Article
- Preoperative inflammatory pain exacerbates postoperative pain and neurocognitive impairment.IBRO neuroscience reports · 2025Article
- Nicotine Attenuates Chondrocyte Inflammation via the α7nAChR-Mediated Inhibition of the HMGB1/TLR4/NF-κB Signaling Pathway.Journal of inflammation research · 2025Article
- Potential pharmaceuticals targeting neuroimmune interactions in treating acute lung injury.Clinical and translational medicine · 2024Review
- HMGB1 as an extracellular pro-inflammatory cytokine: Implications for drug-induced organic damage.Cell biology and toxicology · 2024Review
- Cholinergic α7 nAChR signaling suppresses SARS-CoV-2 infection and inflammation in lung epithelial cells.Journal of molecular cell biology · 2024Article
- The multifunctional protein HMGB1: 50 years of discovery.Nature reviews. Immunology · 2023Review
- Article
- Outcomes of nicotinic modulation on markers of intestinal IgA antibody response.Biomedical reports · 2023Article
- Potential uses of auditory nerve stimulation to modulate immune responses in the inner ear and auditory brainstem.Frontiers in integrative neuroscience · 2023Article
- Review
- Dual effects of supplemental oxygen on pulmonary infection, inflammatory lung injury, and neuromodulation in aging and COVID-19.Free radical biology & medicine · 2022Review
- Nicotinic receptors modulate antitumor therapy response in triple negative breast cancer cells.World journal of clinical oncology · 2022Article
- Selective Agonists and Antagonists of α9 Versus α7 Nicotinic Acetylcholine Receptors.ACS chemical neuroscience · 2022Article
- Peripheral nerve stimulation and immunity: the expanding opportunities for providing mechanistic insight and therapeutic intervention.International immunology · 2022Review
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Authors and funding
12 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundOxygen therapy, using supraphysiological concentrations of oxygen (hyperoxia), is routinely administered to patients who require respiratory support including mechanical ventilation (MV). However, prolonged exposure to hyperoxia results in acute lung injury (ALI) and accumulation of high mobility group box 1 (HMGB1) in the airways. We previously showed that airway HMGB1 mediates hyperoxia-induced lung injury in a mouse model of ALI. Cholinergic signaling through the α7 nicotinic acetylcholine receptor (α7nAChR) attenuates several inflammatory conditions. The aim of this study was to determine whether 3-(2,4 dimethoxy-benzylidene)-anabaseine dihydrochloride, GTS-21, an α7nAChR partial agonist, inhibits hyperoxia-induced HMGB1 accumulation in the airways and circulation, and consequently attenuates inflammatory lung injury.
methodsMice were exposed to hyperoxia (≥99% O
resultsThe systemic administration of GTS-21 (4 mg/kg) significantly decreased levels of HMGB1 in the airways and the serum. Moreover, GTS-21 (4 mg/kg) significantly reduced hyperoxia-induced acute inflammatory lung injury, as indicated by the decreased total protein content in the airways, reduced infiltration of inflammatory monocytes/macrophages and neutrophils into the lung tissue and airways, and improved lung injury histopathology.
conclusionsOur results indicate that GTS-21 can attenuate hyperoxia-induced ALI by inhibiting extracellular HMGB1-mediated inflammatory responses. This suggests that the α7nAChR represents a potential pharmacological target for the treatment regimen of oxidative inflammatory lung injury in patients receiving oxygen therapy.
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