Frontiers in endocrinology · 2025
Exploring the potential association and experimental validation of disrupted circadian rhythms with polycystic ovary syndrome via meta-analysis and bioinformatics: a possible pathogenic mechanism.
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Li Wenjia, Zhang Guanmei, Fang Yue, Wu Siyi, Song Xiaobo, Zhou Lushan, Lei Lei, Wang Chenye, Ding Caifei, Wang Yixuan
Аннотация
BACKGROUND: Polycystic ovary syndrome (PCOS) has been extensively studied as a common female endocrine disease. In recent years, the relationship between circadian rhythm and PCOS has gradually drawn attention, although the precise nature of this connection remains unclear. The aim of this study was to explore further links between circadian rhythm and PCOS and to identify potential mediators of the pathogenesis of PCOS.
METHOD: We analyzed the available data on PCOS and circadian rhythm disorders. Consequently, we identified potential transcription factors (NPAS2, INSIG1, H3F3B, SCML1) through bioinformatics and verified them in a well-established PCOS mouse model.
RESULTS: Luteinizing hormone (LH), testosterone (T), and melatonin (ML) exhibited substantial changes in the PCOS patients compared to healthy controls, with ML serving as a crucial biomarker in circadian rhythms. PCR results from ovarian tissues demonstrated altered expression of circadian core oscillator in the PCOS mouse model, with NPAS2 expression aligning with the bioinformatics analysis trend. We used quercetin (QUE) as a treatment and observed that it improved the disturbed expression of circadian core oscillations.
CONCLUSION: Our research revealed the correlation between circadian rhythm disruptions and PCOS, identified potential targets, and provided unique insights into the pathogenesis of circadian rhythm-related PCOS. The improvement of circadian core oscillations in the QUE group offers a novel strategy for the treatment of PCOS.
METHOD: We analyzed the available data on PCOS and circadian rhythm disorders. Consequently, we identified potential transcription factors (NPAS2, INSIG1, H3F3B, SCML1) through bioinformatics and verified them in a well-established PCOS mouse model.
RESULTS: Luteinizing hormone (LH), testosterone (T), and melatonin (ML) exhibited substantial changes in the PCOS patients compared to healthy controls, with ML serving as a crucial biomarker in circadian rhythms. PCR results from ovarian tissues demonstrated altered expression of circadian core oscillator in the PCOS mouse model, with NPAS2 expression aligning with the bioinformatics analysis trend. We used quercetin (QUE) as a treatment and observed that it improved the disturbed expression of circadian core oscillations.
CONCLUSION: Our research revealed the correlation between circadian rhythm disruptions and PCOS, identified potential targets, and provided unique insights into the pathogenesis of circadian rhythm-related PCOS. The improvement of circadian core oscillations in the QUE group offers a novel strategy for the treatment of PCOS.