ReviewPharmaceuticals (Basel, Switzerland)2024
Dysregulation of the Arachidonic Acid Pathway in Cystic Fibrosis: Implications for Chronic Inflammation and Disease Progression.
Review in Pharmaceuticals (Basel, Switzerland), 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 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
8 citing papers in PubMed.
- Association Between Complete Blood Count and the Lipoxygenase Pathway in Hashimoto's Thyroiditis.Cells · 2025Article
- Arachidonic acid protects against diabetes-induced atrial fibrillation.Lipids in health and disease · 2025Article
- Comparative Single-Cell Transcriptomics Uncovers Shared and Distinct Molecular Signatures in Cystic Fibrosis and Primary Ciliary Dyskinesia.bioRxiv : the preprint server for biology · 2025Article
- Article
- Cystic fibrosis and inflammatory bowel disease: parallels in gut physiology and microbiota.Journal of bacteriology · 2025Review
- Redox Imbalance in Cystic Fibrosis: The Multifaceted Role of Oxidative Stress.Pharmaceuticals (Basel, Switzerland) · 2025Review
- Review
- CP1Hao Decoction Alleviates Chronic Prostatitis by Modulating Arachidonic Acid Metabolism: A Multi-Omics Analysis.American journal of men's healthArticle
Corrections and comments
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Authors and funding
2 authors.
Funding
Abstract
Cystic fibrosis (CF) is the most common fatal genetic disease among Caucasian people, with over 2000 mutations in the CFTR gene. Although highly effective modulators have been developed to rescue the mutant CFTR protein, unresolved inflammation and persistent infections still threaten the lives of patients. While the central role of arachidonic acid (AA) and its metabolites in the inflammatory response is widely recognized, less is known about their impact on immunomodulation and metabolic implications in CF. To this end, here we provided a comprehensive analysis of the AA metabolism in CF. In this context, CFTR dysfunction appeared to complexly disrupt normal lipid processing, worsening the chronic airway inflammation, and compromising the immune responses to bacterial infections. As such, potential strategies targeting AA and its inflammatory mediators are being investigated as a promising approach to balance the inflammatory response while mitigating disease progression. Thus, a deeper understanding of the AA pathway dysfunction in CF may open innovative avenues for designing more effective therapeutic interventions.
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Registered trials
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