Mitochondria and polycystic ovary syndrome: The role of ferroptosis, inflammasomes, and endoplasmic reticulum stress
Abstract
Polycystic ovary syndrome (PCOS) poses a major threat to women of reproductive age and is strongly associated with metabolic and inflammatory abnormalities. Over the past decade, tremendous progress has been made in our understanding of signaling events regulated by mitochondria. Emerging evidence underscores mitochondrial dysfunction as a central pathophysiological hub in PCOS. The intricate crosstalk among mitochondrial dysfunction, ferroptosis, inflammasomes, and endoplasmic reticulum (ER) stress creates a pathological network that underpins ovarian dysfunction, metabolic abnormalities, and chronic inflammation in PCOS, highlighting promising novel targets for diagnosis and therapeutic intervention in this complex disorder.
Fields of Study & Subjects
Ferroptosis and cancer prognosis
GDF15 and Related Biomarkers
Clusterin in disease pathology
Publication details
- Journal / source
- International Journal of Biological Sciences
- Publisher
- Ivyspring International Publisher
- Volume
- 22
- Issue
- 9
- Pages
- 4938–4955
- Publication date
- 1 May 2026
- Language
- EN