Abstract
Polycystic ovarian syndrome (PCOS) is the most common endocrine–metabolic disorder affecting a vast population worldwide; it is linked with anovulation, mitochondrial dysfunctions and hormonal disbalance. Mutations in mtDNA have been identified in PCOS patients and likely play an important role in PCOS aetiology and pathogenesis; however, their causative role in PCOS development requires further investigation. As a low-grade chronic inflammation disease, PCOS patients have permanently elevated levels of inflammatory markers (TNF-α, CRP, IL-6, IL-8, IL-18). In this review, we summarise recent data regarding the role of mtDNA mutations and mitochondrial malfunctions in PCOS pathogenesis. Furthermore, we discuss recent papers dedicated to the identification of novel biomarkers for early PCOS diagnosis. Finally, traditional and new mitochondria-targeted treatments are discussed. This review intends to emphasise the key role of oxidative stress and chronic inflammation in PCOS pathogenesis; however, the exact molecular mechanism is mostly unknown and requires further investigation.
Highlights
Stein–Leventhal syndrome, commonly known as polycystic ovarian syndrome (PCOS), is a complex, multifaceted endocrine disease with a global prevalence among women of reproductive age
We have summarised the mtDNA mutations identified in Polycystic ovarian syndrome (PCOS) patients (Table 1)
The data presented above suggest that mitochondrial dysfunction is involved in PCOS
Summary
Stein–Leventhal syndrome, commonly known as polycystic ovarian syndrome (PCOS), is a complex, multifaceted endocrine disease with a global prevalence among women of reproductive age. Mitochondria are the central player in energy production and the main source of cellular ROS (reactive oxygen species), leading to OS (oxidative stress) damage Due to this reason, mitochondrial abnormalities often have organism-wide manifestation and result in different metabolic disorders [13]. The level of the hormone leptin, mostly produced by adipose tissue, is elevated in PCOS patients; it upregulates INF-γ (interferon-gamma) and IL-6 production and binds with IR [36]. These data represent a crucial connection between the metabolic manifestation of PCOS and chronic inflammation. We will summarise recent achievements in understanding the role of mitochondrial mutations and chronic inflammation in PCOS pathogenesis and novel targets in PCOS therapy and diagnosis
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