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Repurposing Belinostat for Alleviation of Atopic Dermatitis
Shan Quah1, Gowtham Subramanian1, Prabha Sampath2,3
1Skin Research Institute of Singapore, Agency for Science Technology and Research (A*STAR), 138648, Singapore, Singapore.
Atopic dermatitis (AD) involves skin barrier defects linked to lost miR-335. Belinostat, a histone deacetylase inhibitor, can restore miR-335 and improve skin barrier function in AD models.
Area of Science:
- Dermatology and immunology
- Epigenetics and non-coding RNA research
Background:
- Atopic dermatitis (AD) is a chronic inflammatory skin condition with significant impact on quality of life.
- Pathophysiology involves immune responses and skin barrier defects, with mechanisms not fully elucidated.
- miR-335, a microRNA, is crucial for keratinocyte differentiation and skin barrier integrity.
Discussion:
- miR-335 expression is reduced in AD, contributing to skin barrier dysfunction.
- Histone deacetylase inhibitors, such as belinostat, show potential in restoring miR-335 levels.
- Belinostat effectively resolved skin barrier defects in a dry skin model.
Key Insights:
- Loss of miR-335 is a key factor in AD-related skin barrier defects.
- Belinostat demonstrates therapeutic potential by restoring miR-335 and skin barrier function.
- The study highlights the interplay between epigenetic regulation and non-coding RNAs in AD.
Outlook:
- Further research is needed on the crosstalk between epigenetic and non-coding RNA regulation in AD.
- Exploring epigenome-targeting therapeutic strategies for AD is a promising avenue.
- Investigating belinostat's efficacy and safety in clinical AD settings is warranted.
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