Department of Medical and Clinical Biochemistry, Faculty of Medicine, Pavol Jozef Šafárik University in Košice, Trieda SNP 1, 040 11 Košice, Slovakia.
Department of Gynaecology and Obstetrics, Faculty of Medicine, Pavol Jozef Šafárik University in Košice, Trieda SNP 1, 040 11 Košice, Slovakia.
Cells. 2024 Jun 22;13(13):1081. doi: 10.3390/cells13131081.
Successful pregnancy depends on precise molecular regulation of uterine physiology, especially during the menstrual cycle. Deregulated oxidative stress (OS), often influenced by inflammatory changes but also by environmental factors, represents a constant threat to this delicate balance. Oxidative stress induces a reciprocally regulated nuclear factor erythroid 2-related factor 2/peroxisome proliferator-activated receptor-gamma (Nrf2/PPARγ) pathway. However, increased PPARγ activity appears to be a double-edged sword in endometrial physiology. Activated PPARγ attenuates inflammation and attenuates OS to restore redox homeostasis. However, it also interferes with physiological processes during the menstrual cycle, such as hormonal signaling and angiogenesis. This review provides an elucidation of the molecular mechanisms that support the interplay between PPARγ and OS. Additionally, it offers fresh perspectives on the Nrf2/PPARγ pathway concerning endometrial receptivity and its potential implications for infertility.
成功的妊娠取决于子宫生理学的精确分子调控,尤其是在月经周期期间。氧化应激(OS)失调,通常受炎症变化影响,但也受环境因素影响,对这种微妙的平衡构成持续威胁。氧化应激诱导核因子红细胞 2 相关因子 2/过氧化物酶体增殖物激活受体-γ(Nrf2/PPARγ)途径的反向调节。然而,PPARγ 活性的增加在子宫内膜生理学中似乎是一把双刃剑。激活的 PPARγ 可减轻炎症和氧化应激,以恢复氧化还原平衡。然而,它也会干扰月经周期中的生理过程,如激素信号和血管生成。本综述阐述了支持 PPARγ 和 OS 相互作用的分子机制。此外,它还提供了关于 Nrf2/PPARγ 途径的新视角,涉及子宫内膜容受性及其对不孕的潜在影响。