Fig. 3

OS-related signaling pathways in ovarian aging. Excess levels of ROS promote the dissociation of the Keap1-Nrf2 complex and Nrf2 translocation into the nucleus to bind to AREs, thus promoting the expression of antioxidant enzymes. Sirt can deacetylate key proteins involved in the cellular stress response such as FoxO, and regulate both telomerase activity and mitochondrial function through PGC1α. The MAPK cascade signaling pathway is activated by ROS to deliver extracellular signals to the nucleus, promote apoptosis, inhibit proliferation and induce cell cycle arrest. AKT plays an important role in the regulation of cellular redox homeostasis, and phosphorylated AKT can regulate a variety of downstream proteins (Bad, mTOR, Cyclins and Nrf2) to further regulate cellular apoptosis, autophagy and proliferation. FoxO senses cellular OS status and acts as a transcription factor to regulate cell apoptosis and the expression of antioxidant enzymes. Klotho regulates cellular oxidative homeostasis through the PI3K/AKT pathway, and the HPO axis through the FGF-Klotho endocrine system