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Exploring the Potential Role of Hydroxytyrosol in Androgenetic Alopecia: An Integrated Bioinformatics and Molecular
Leying Zhang1, Xiaoyang An1, Meihong Xu1,2
1Department of Nutrition and Food Hygiene, School of Public Health, Beijing Key Laboratory of Toxicological Research and Risk Assessment for Food Safety, Peking University, Beijing 100191, China.
International Journal of Molecular Sciences
|June 12, 2026
Summary
Hydroxytyrosol (HT) may help treat androgenetic alopecia (AGA) by reducing inflammation and oxidative stress. This study identified key genes and pathways modulated by HT, suggesting potential therapeutic mechanisms for AGA.
Area of Science:
- Molecular Biology
- Pharmacology
- Dermatology
Background:
- Androgenetic alopecia (AGA) involves follicular miniaturization, oxidative stress, and microinflammation.
- Hydroxytyrosol (HT) possesses known antioxidant and anti-inflammatory properties, but its role in AGA is not fully understood.
Purpose of the Study:
- To investigate the molecular mechanisms of Hydroxytyrosol (HT) in androgenetic alopecia (AGA).
- To identify potential therapeutic targets of HT for AGA treatment.
Main Methods:
- Bioinformatic analysis of differentially expressed genes (DEGs) from GSE212301 dataset.
- Intersection of DEGs with predicted HT targets to identify candidate genes.
- Pathway enrichment analysis, protein-protein interaction (PPI) network construction, and hub gene identification.
- Molecular docking and molecular dynamics (MD) simulations to assess HT binding affinity and stability with target proteins.
Main Results:
- Identified 506 DEGs and 24 candidate targets of HT relevant to AGA.
- Enrichment analysis revealed involvement of MAPK, NF-κB, TNF, and HIF-1 signaling pathways.
- Identified HMOX1, PTGS2, FOS, and JUN as key hub genes.
- Molecular docking and MD simulations indicated favorable binding and stability of HT with PTGS2.
Conclusions:
- Hydroxytyrosol (HT) may exert therapeutic effects in androgenetic alopecia (AGA) by modulating inflammatory and oxidative stress pathways.
- HMOX1 and PTGS2 are identified as crucial targets for HT's action in AGA.
- Findings provide a foundation for further experimental validation of HT as a potential AGA treatment.