Targeting Interleukin-17 as a Novel Treatment Option for Fibrotic Diseases
Margherita Sisto1, Sabrina Lisi1
1Department of Translational Biomedicine and Neuroscience (DiBraiN), Section of Human Anatomy and Histology, University of Bari "Aldo Moro", 70124 Bari, Italy.
Journal of Clinical Medicine
|January 11, 2024
Summary
Fibrosis, a major cause of organ failure, is linked to elevated interleukin-17 (IL-17). New research explores epigenetic control of IL-17 to develop antifibrotic therapies.
Area of Science:
- Immunology
- Pathology
- Molecular Biology
Background:
- Fibrosis is a significant cause of organ damage and mortality worldwide, often stemming from chronic inflammation.
- Currently, antifibrotic treatment options are limited, highlighting an unmet medical need.
- Elevated levels of interleukin-17 (IL-17) are increasingly implicated in chronic inflammatory conditions leading to fibrotic complications and organ failure.
Purpose of the Study:
- To review the current understanding of interleukin-17 (IL-17)'s role in the development of fibrotic diseases.
- To highlight recent advancements in therapeutic strategies targeting IL-17 pathways in fibrosis.
- To explore the potential of epigenetic mechanisms in controlling IL-17 levels for antifibrotic treatments.
Main Methods:
- Literature review focusing on the role of IL-17 in fibrotic diseases.
- Analysis of recent research on therapeutic interventions targeting IL-17.
- Examination of epigenetic mechanisms influencing IL-17 expression in fibrotic contexts.
Main Results:
- IL-17 plays a critical role in the pathogenesis of various fibrotic diseases.
- Emerging research focuses on epigenetic modifications as key regulators of IL-17 in fibrosis.
- Targeting IL-17 signaling pathways, particularly through epigenetic modulation, shows promise for novel antifibrotic therapies.
Conclusions:
- Understanding the IL-17 signaling pathway is crucial for developing effective antifibrotic strategies.
- Epigenetic mechanisms offer a promising avenue for therapeutic intervention in IL-17-driven fibrosis.
- Further research into IL-17 and its epigenetic regulation could lead to significant advancements in treating fibrotic diseases.
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