Level D· Scientific groundwork from lab and animal studiesNarrative ReviewEurope PMCOpen access

Unraveling mitochondrial dysfunction in polycystic ovary syndrome: Pathophysiological insights

Li CJ., Lin LT., Lin PH., Chen YC., Lin PW., Wen ZH.

Narrative Review on Type 2 Diabetes, Chronic Inflammation, published in J Chin Med Assoc (2025) — summary generated from the PubMed abstract.

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Level D· Scientific groundwork from lab and animal studiesEvidence level of this study

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

  • Level A · Stronger Clinical Evidence
  • Level B · Emerging clinical evidence with positive signals
  • Level C · Early human research exploring benefits
  • Level D · Scientific groundwork from lab and animal studies
  • Emerging · Emerging topic under active research
Read the A–D evidence level guide

This page is generated from the PubMed record. The Thai description is an automated summary of bibliographic fields and the abstract, not a full translation, and is not medical advice.

Study type
Narrative Review
Journal
J Chin Med Assoc (2025)
Reported sample size
—
Source database
Europe PMC
PMID
40813993
PMCID
PMC12742714
DOI
10.1097/jcma.0000000000001281

Abstract (original English)

Polycystic ovary syndrome (PCOS) is a common endocrine and metabolic disorder that affects women of reproductive age. It is characterized by ovulatory dysfunction, excessive levels of androgens, and the presence of multiple cysts in the ovaries. Although the exact cause of PCOS remains uncertain, recent studies have identified mitochondrial dysfunction as a key contributing factor. Mitochondria, often described as the energy centers of the cell, are essential for producing ATP, generating reactive oxygen species (ROS), and regulating cell death pathways. A growing body of evidence shows that mitochondrial dysfunction occurs in the ovaries, skeletal muscle, and adipose tissue of individuals with PCOS. This dysfunction may play a central role in the development of the disorder by increasing oxidative stress and chronic inflammation, worsening insulin resistance, and interfering with oocyte growth and quality. This review summarizes recent progress in understanding how mitochondrial dysfunction contributes to the underlying biology of PCOS. It also explores emerging treatment strategies that aim to restore mitochondrial health, such as the use of antioxidants, therapies that specifically target mitochondria, and emerging mitochondrial replacement technologies. These approaches hold promise for reducing the symptoms and long-term complications associated with PCOS.

What this study does not prove

  • • This study does not prove SVF is an approved treatment or a replacement for standard care.
  • • This is a narrative review: it collects no new patient data and does not systematically appraise evidence quality.

Evidence level

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

How we grade evidence
MitochondriaHumansPolycystic Ovary SyndromeInsulin ResistanceReactive Oxygen SpeciesOxidative StressFemale

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