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Pathophysiological roles of chronic low‐grade inflammation mediators in polycystic ovary syndrome
Author(s) -
Rostamtabar Maryam,
Esmaeilzadeh Sedigheh,
Tourani Mehdi,
Rahmani Abolfazl,
Baee Masoud,
Shirafkan Fatemeh,
Saleki Kiarash,
Mirzababayi Sajedeh S.,
Ebrahimpour Soheil,
Nouri Hamid Reza
Publication year - 2021
Publication title -
journal of cellular physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.529
H-Index - 174
eISSN - 1097-4652
pISSN - 0021-9541
DOI - 10.1002/jcp.29912
Subject(s) - polycystic ovary , inflammation , medicine , insulin resistance , inflammasome , immunology , pathophysiology , disease , immune system , infertility , endocrinology , biology , insulin , pregnancy , genetics
Polycystic ovary syndrome (PCOS) is the most common hormonal imbalance disease in reproductive‐aged women. Its basic characteristics are ovulatory dysfunction and ovarian overproduction of androgens that lead to severe symptoms such as insulin resistance, hirsutism, infertility, and acne. Notwithstanding the disease burden, its underlying mechanisms remain unknown, and no causal therapeutic exists. In recent years, further studies showed that inflammation processes are involved in ovulation and play a key role in ovarian follicular dynamics. Visceral adipose tissue can cause inflammatory response and maintenance of the inflammation state in adipocytes by augmented production of inflammatory cytokines, monocyte chemoattractant proteins, and recruitment of the immune cell. Therefore, the PCOS can be related to a low‐grade inflammation state and inflammatory markers. Investigating the inflammatory processes and mediators that contribute to the commencement and development of PCOS can be a critical step for better understanding the pathophysiology of the disease and its treatment through inhibition or control of related pathways. In the present review, we discuss the pathophysiological roles of chronic low‐grade inflammation mediators including inflammasome‐related cytokines, interleukin‐1β (IL‐1β), and IL‐18 in PCOS development.