Oxidative Stress and the Nrf2/PPARγ Axis in the Endometrium: Insights into Female Fertility

• Published in: Cells (Basel, Switzerland) Vol. 13; no. 13; p. 1081
• Main Authors: Artimovič, Peter, Badovská, Zuzana, Toporcerová, Silvia, Špaková, Ivana, Smolko, Lukáš, Sabolová, Gabriela, Kriváková, Eva, Rabajdová, Miroslava
• Format: Journal Article
• Language: English
• Published: Switzerland MDPI AG 22-06-2024
• Subjects: Angiogenesis; Animals; Apoptosis; Blood vessels; cellular signaling; Chemokines; Cytokines; Endometrium; Endometrium - metabolism; Environmental factors; Enzymes; Estrogens; Female; Females; Fertility; Fertility - physiology; Homeostasis; Humans; In vitro fertilization; Infertility; Inflammation; Kinases; Menstrual cycle; Menstruation; Molecular modelling; Morphology; NF-E2-Related Factor 2 - metabolism; Nitric oxide; Nrf2; Ovaries; Ovulation; Oxidative Stress; Peroxisome proliferator-activated receptors; Physiology; Polycystic ovary syndrome; PPAR gamma - metabolism; PPARγ; Signal Transduction; Transcription factors; Nrf2; fertility; cellular signaling; endometrium; mini review; female; PPARγ; oxidative stress
• ISSN: 2073-4409; 2073-4409
• 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.