Key result
Endoplasmic reticulum stress and the unfolded protein response are upregulated in polycystic ovary syndrome and may play a key role in its complex pathophysiology and associated ovarian outcomes.
This review highlights the potential role of endoplasmic reticulum stress and the unfolded protein response in the pathophysiology of polycystic ovary syndrome.
May link ER stress to PCOS ovarian dysfunction; hypothesis-generating for UPR-targeted interventions pending prospective trials.
Polycystic ovary syndrome (PCOS) is an endocrine disorder that affects million women worldwide, presenting a complex pathophysiology that has not been fully elucidated yet. Recently, it has been suggested that PCOS triggers the endoplasmic reticulum (ER) stress, thus being associated with unfolded protein response (UPR) activation. Indeed, the UPR response has been associated with several pathological conditions, including in the reproductive system. Several studies demonstrated that ovarian UPR markers are upregulated in PCOS, being associated with worst ovarian outcomes, and this was ameliorated by ER stress inhibition. In this review, we aim to summarize the main findings from previous studies covering this topic, in an attempt to clarify the potential role of ER stress and the UPR response in the pathophysiology of PCOS.
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Alexandre‐Santos et al. (2022) conducted a review in Polycystic ovary syndrome (PCOS). Endoplasmic reticulum (ER) stress and unfolded protein response (UPR) was evaluated. Endoplasmic reticulum stress and the unfolded protein response are upregulated in polycystic ovary syndrome and may play a key role in its complex pathophysiology and associated ovarian outcomes.
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