ArticleMediators of inflammation2013
Contribution of CFTR to alveolar fluid clearance by lipoxin A4 via PI3K/Akt pathway in LPS-induced acute lung injury.
Article in Mediators of inflammation, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers, 1 of them a synthesis that pooled it.
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Who cites it
24 citing papers in PubMed, 1 synthesis or guideline pooled it, 41 citations in OpenAlex.
- The role of fatty acid metabolism in acute lung injury: a special focus on immunometabolism.Cellular and molecular life sciences : CMLS · 2024Pooled it
- Evaluation of the Effects of Lipoxin A4 and Resolvin D1 on the Severity of Transient Tachypnea of the Newborn: A Prospective Study.Children (Basel, Switzerland) · 2025Article
- The potential of exogenous specialized pro-resolving mediators in protecting against sepsis-associated lung injury: a review.Frontiers in pharmacology · 2025Review
- Influence of SphK1 on Inflammatory Responses in Lipopolysaccharide-Challenged RAW 264.7 Cells.Cell biochemistry and biophysics · 2024Article
- An ex vivo rat trachea model reveals abnormal airway physiology and a gland secretion defect in cystic fibrosis.PloS one · 2023Article
- The Effect and Mechanism of Lipoxin A4 on Neutrophil Function in LPS-Induced Lung Injury.Inflammation · 2022Article
- Review of the potential of mesenchymal stem cells for the treatment of infectious diseases.World journal of stem cells · 2021Review
- Specialized proresolving mediators in infection and lung injury.BioFactors (Oxford, England) · 2021Review
- Resolution-Based Therapies: The Potential of Lipoxins to Treat Human Diseases.Frontiers in immunology · 2021Review
- LXA4 Inhibits Lipopolysaccharide-Induced Inflammatory Cell Accumulation by Resident Macrophages in Mice.Journal of inflammation research · 2021Article
- The Role of Specialized Pro-Resolving Mediators in Cystic Fibrosis Airways Disease.Frontiers in pharmacology · 2020Review
- Annexin A1 Mimetic Peptide AC2-26 Inhibits Sepsis-induced Cardiomyocyte Apoptosis through LXA4/PI3K/AKT Signaling Pathway.Current medical science · 2018Article
- Specialized Pro-resolving Mediators Regulate Alveolar Fluid Clearance during Acute Respiratory Distress Syndrome.Chinese medical journal · 2018Review
- pre-B cell colony enhancing factor negatively regulates NaAmerican journal of translational research · 2018Article
- Insulin signaling via the PI3-kinase/Akt pathway regulates airway glucose uptake and barrier function in a CFTR-dependent manner.American journal of physiology. Lung cellular and molecular physiology · 2017Article
- Lipoxin A4 pretreatment mitigates skeletal muscle ischemia-reperfusion injury in rats.American journal of translational research · 2017Article
- The role of stretch-activated ion channels in acute respiratory distress syndrome: finally a new target?American journal of physiology. Lung cellular and molecular physiology · 2016Review
- Mesenchymal stem cells ameliorate inflammatory cytokine-induced impairment of AT-II cells through a keratinocyte growth factor-dependent PI3K/Akt/mTOR signaling pathway.Molecular medicine reports · 2016Article
- Increased TMEM16A Involved in Alveolar Fluid Clearance After Lipopolysaccharide Stimulation.Inflammation · 2016Article
- Modulation of the Activities of Neuronal Ion Channels by Fatty Acid-Derived Pro-Resolvents.Frontiers in physiology · 2016Review
Corrections and comments
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Authors and funding
11 authors at 1 institution in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The lipoxins are the first proresolution mediators to be recognized and described as the endogenous "braking signals" for inflammation. We evaluated the anti-inflammatory and proresolution bioactions of lipoxin A4 in our lipopolysaccharide (LPS-)induced lung injury model. We demonstrated that lipoxin A4 significantly improved histology of rat lungs and inhibited IL-6 and TNF- α in LPS-induced lung injury. In addition, lipoxin A4 increased alveolar fluid clearance (AFC) and the effect of lipoxin A4 on AFC was abolished by CFTRinh-172 (a specific inhibitor of CFTR). Moreover, lipoxin A4 could increase cystic fibrosis transmembrane conductance regulator (CFTR) protein expression in vitro and in vivo. In rat primary alveolar type II (ATII) cells, LPS decreased CFTR protein expression via activation of PI3K/Akt, and lipoxin A4 suppressed LPS-stimulated phosphorylation of Akt. These results showed that lipoxin A4 enhanced CFTR protein expression and increased AFC via PI3K/Akt pathway. Thus, lipoxin A4 may provide a potential therapeutic approach for acute lung injury.
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