Fig. 6

Stem cell exhaustion and intercellular communication regulated by redox signaling. a Cellular senescence typically facilitates tissue repair following injury and shields the organism from oncogenic harm. This process occurs through four sequential steps: damage, senescence, elimination, and repair. Failure in each of these steps renders the organism susceptible to developing diseases. b The stemness of cells is regulated by multiple pathways. Among them, the redox modification of Keap1 regulates the stability of NRF2, thereby modulating the expression of its downstream effectors Notch1 and Shh. Notch1 and Shh serve as ligands of the Notch and Hedgehog pathways, respectively, and their activation is crucial for maintaining cellular stemness. In the Wnt pathway, FOXO is subjected to redox regulation, affecting the transcription of β-catenin. The TGF-β pathway is also implicated in cellular stemness. c The redox signaling pathways regulate extracellular signaling pathways. TGF-β and integrins respectively modulate the activation of p38 and ERK, thereby regulating the proliferation and survival of tumor cells. The Hippo signaling pathway is regulated by adherens junctions, tight junctions, and CRB, which prevent nuclear translocation by binding to phosphorylated YAP. GPCRs and integrins can regulate the actin cytoskeleton, and inhibit the process of the Hippo kinase core, thereby reducing YAP phosphorylation, promoting its nuclear translocation, and regulating organ size, cell survival, and proliferation