Abstract:

The aberrant expression of adipokines may contribute to the onset and progression of polycystic ovary syndrome (PCOS), with its mechanism involving the regulation of multiple signaling pathways including Wnt/β-catenin, phosphatidylinositol 3-kinase (PI3K)/protein kinase B (Akt), c-Jun N-terminal kinase (JNK) /mitogen-activated protein kinase (MAPK), Janus kinase (JAK)/signal transducer and activator of transcription (STAT), nuclear factor-κB (NF-κB) and their downstream signaling molecules. Research indicates that various therapeutic modalities, such as exogenous adipokines, specific adipokine antagonists, conventional hypoglycemic agents and dietary interventions, can ameliorate PCOS-related ovarian pathology, modulate insulin signal transduction and the expression of genes associated with hormone synthesis, suppress oxidative stress and inflammatory reactions, enhance endometrial receptivity, and facilitate embryo implantation and development by rectifying the expression of adipokines and their receptors. In turn, these interventions alleviate PCOS-related endocrine and metabolic disturbances, immune abnormalities, and reproductive dysfunctions. Adipokines may be as a potential target for the PCOS treatment. Nevertheless, owing to the intricate crosstalk between adipokines and the substantial heterogeneity among PCOS patients, current research primarily centers on animal studies. Based on these animal studies, additional clinical trials should be well designed to develope the innovative regimens of PCOS treatment based on adipokine regulation.

Key words: Polycystic ovary syndrome, Adipokines, Molecular targeted therapy, Molecular mechanisms, Exogenous adipokines, Adipokine antagonist