PDF(Pubmed)
Abstract：
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.
摘要：
成功的怀孕取决于子宫生理的精确分子调节，尤其是在月经周期。解除氧化应激(OS)，通常受炎症变化的影响，也受环境因素的影响，代表着对这种微妙平衡的持续威胁。氧化应激诱导相互调节的核因子红系2相关因子2/过氧化物酶体增殖物激活受体γ（Nrf2/PPARγ）途径。然而,PPARγ活性增加似乎是子宫内膜生理学中的一把双刃剑。激活的PPARγ减弱炎症并减弱OS以恢复氧化还原稳态。然而,它也会干扰月经周期的生理过程，如激素信号和血管生成。这篇综述阐明了支持PPARγ和OS相互作用的分子机制。此外,它提供了有关子宫内膜容受性的Nrf2/PPARγ途径及其对不孕症的潜在影响的新观点。
