Version 1
: Received: 25 July 2023 / Approved: 26 July 2023 / Online: 26 July 2023 (11:29:11 CEST)
Version 2
: Received: 18 August 2023 / Approved: 21 August 2023 / Online: 21 August 2023 (10:16:55 CEST)
Siemers, K.M.; Klein, A.K.; Baack, M.L. Mitochondrial Dysfunction in PCOS: Insights into Reproductive Organ Pathophysiology. Int. J. Mol. Sci.2023, 24, 13123.
Siemers, K.M.; Klein, A.K.; Baack, M.L. Mitochondrial Dysfunction in PCOS: Insights into Reproductive Organ Pathophysiology. Int. J. Mol. Sci. 2023, 24, 13123.
Siemers, K.M.; Klein, A.K.; Baack, M.L. Mitochondrial Dysfunction in PCOS: Insights into Reproductive Organ Pathophysiology. Int. J. Mol. Sci.2023, 24, 13123.
Siemers, K.M.; Klein, A.K.; Baack, M.L. Mitochondrial Dysfunction in PCOS: Insights into Reproductive Organ Pathophysiology. Int. J. Mol. Sci. 2023, 24, 13123.
Abstract
Polycystic ovary syndrome (PCOS) is a complex, but relatively common endocrine disorder associated with chronic anovulation, hyperandrogenism, and micro-polycystic ovaries [1]. In addition to reduced fertility, people with PCOS have a higher risk of obesity, insulin resistance, and metabolic disease [1], all comorbidities that are associated with mitochondrial dysfunction. This review summarizes human and animal data that report mitochondrial dysfunction and metabolic dysregulation in PCOS to better understand how mitochondria impact reproductive organ pathophysiology. This in-depth review considers all the elements regulating mitochondrial quantity and quality, from mitochondrial biogenesis under transcriptional regulation of both the nuclear and the mitochondrial genome, to the ultrastructural and functional complexes that regulate cellular metabolism and reactive oxygen species production, to dynamics which regulate subcellular interactions that are key to mitochondrial quality control. When any of these mitochondrial functions are disrupted the energetic equilibrium within the cell changes, cell processes can fail, and cell death can occur. If this process is ongoing, it affects tissue and organ function to cause disease. The objective of this review is to consolidate and classify a broad number of PCOS studies to understand how various mitochondrial processes impact reproductive organs including the ovary (oocyte and granulosa cell), uterus, placenta, and circulation to cause reproductive pathophysiology. A secondary objective is to uncover the potential role of mitochondria in transgenerational transmission of PCOS and metabolic disorders.
Biology and Life Sciences, Endocrinology and Metabolism
Copyright:
This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
Received:
21 August 2023
Commenter:
Michelle Baack
Commenter's Conflict of Interests:
Author
Comment:
Tables were reformatted for easier reading. Study methods were added to include the number of articles recovered by our search terms and reasons for exclusions. More conclusive wording about our findings and interpretation was added to the ovary and placenta tissue sections and a Conclusion statement was added to address potential treatments that were not discussed in the review.
Commenter: Michelle Baack
Commenter's Conflict of Interests: Author