| Autor: |
D'Orazio S; Department of Medical, Oral and Biotechnology Sciences, University 'G. d'Annunzio' Chieti-Pescara, 66100 Chieti, Italy.; Center for Advanced Studies and Technology (CAST), University 'G. d'Annunzio' Chieti-Pescara, 66100 Chieti, Italy., Mattoscio D; Department of Medical, Oral and Biotechnology Sciences, University 'G. d'Annunzio' Chieti-Pescara, 66100 Chieti, Italy.; Center for Advanced Studies and Technology (CAST), University 'G. d'Annunzio' Chieti-Pescara, 66100 Chieti, Italy. |
| Jazyk: |
angličtina |
| Zdroj: |
Pharmaceuticals (Basel, Switzerland) [Pharmaceuticals (Basel)] 2024 Sep 09; Vol. 17 (9). Date of Electronic Publication: 2024 Sep 09. |
| DOI: |
10.3390/ph17091185 |
| Abstrakt: |
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. |
| Databáze: |
MEDLINE |
| Externí odkaz: |
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