To determine whether endometrioma fluid (EmF) compromises preantral follicle development through mechanisms involving oxidative stress and tissue fibrosis, potentially contributing to infertility.
Key Findings:
EmF inhibited granulosa cell (GC) proliferation and estradiol production.
EmF increased ROS generation in GC and induced fibrosis markers in TC.
Androgen supplementation partially restored GC proliferation and FSH receptor expression.
Antioxidants, antifibrotic agents, and iron chelators showed no significant effects.
Interpretation:
EmF disrupts preantral follicle development by inducing oxidative stress in GC and promoting fibrosis in TC, which impairs the critical crosstalk between GC and TC, ultimately affecting fertility.
Limitations:
Study limited to a small sample size of patients, which may affect the generalizability of the findings.
Results derived from a rat model may not fully translate to human physiology, necessitating further research.
Conclusion:
The findings reveal a novel pathogenic mechanism underlying endometrioma-associated infertility, highlighting the need for therapeutic strategies targeting oxidative stress and fibrotic remodeling to improve fertility outcomes.
