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Ferroptosis in Recurrent Vulvovaginal Candidiasis Through Integrated Bioinformatics and Experimental Validation
Yue-Min Hou1, Hui Yu2,3, Fang Feng4
1Department of Gynecology and Obstetrics, The Second Affiliated Hospital of Xi 'an Jiaotong University, No.157 Siwu Road, Xi'an 710004, China.
Antioxidants (Basel, Switzerland)
|May 4, 2026
Summary
Recurrent vulvovaginal candidiasis (RVVC) is linked to ferroptosis, a cell death process. Inhibiting ferroptosis with Fer-1 reduced inflammation and fungal burden in models, offering new therapeutic avenues for RVVC.
Area of Science:
- Cellular Biology
- Immunology
- Pathogenesis of Infectious Diseases
Background:
- Recurrent vulvovaginal candidiasis (RVVC) is a chronic inflammatory condition caused by *Candida albicans*, with poorly understood pathogenesis and challenges in treatment due to recurrence and drug resistance.
- Ferroptosis, a form of programmed cell death involving lipid peroxidation, is implicated in various diseases, but its role in RVVC has not been established, particularly lacking clinical and animal data.
Purpose of the Study:
- To investigate the association between RVVC and ferroptosis using clinical data and experimental models.
- To identify ferroptosis-related genes and pathways involved in RVVC pathogenesis.
- To explore ferroptosis as a potential therapeutic target for RVVC.
Main Methods:
- Analysis of high-throughput sequencing data from human RVVC samples (GEO database) and ferroptosis-related genes (FerrDb).
- Construction of protein-protein interaction networks to identify hub genes.
- Validation in a murine model of chronic vulvovaginal candidiasis (CVVC) and an in vitro model of *C. albicans*-infected macrophages.
- Treatment with ferroptosis inhibitor ferrostatin-1 (Fer-1) to assess its effects.
Main Results:
- Identified 194 ferroptosis-related genes and 20 hub genes in RVVC, revealing a
- ferroptosis-inflammation-immunity
- network.
- Found that *C. albicans* infection induces ferroptosis in vaginal tissues and macrophages, impairing antifungal function.
- Fer-1 treatment significantly reduced RVVC pathology, inflammation, fungal burden, and restored immune balance, while preserving macrophage function.
Conclusions:
- This study provides the first evidence linking RVVC to ferroptosis, implicating it in the disease's pathological process.
- Ferroptosis represents a novel perspective for understanding RVVC pathogenesis.
- Targeting ferroptosis may offer new therapeutic strategies for managing RVVC.
