Mitochondria and polycystic ovary syndrome: The role of ferroptosis, inflammasomes, and endoplasmic reticulum stress.

Authors

Xinyi Zhang, Tong Sun, Xinxin Wang, Yujiu Ma, Liu Cao, Jichun Tan

Published in

International journal of biological sciences. Volume 22. Issue 9. Pages 4938-4955. Epub May 01, 2026.

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.

PMID:
42157934
Bibliographic data and abstract were imported from PubMed on 16 Sep 2026.

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