Fig. 3: ROS-mediated regulation of cell cycle progression and associated molecular mechanisms.
From: Immunometabolism and oxidative stress: roles and therapeutic strategies in cancer and aging
This figure illustrates the regulatory roles of ROS in modulating cell cycle phases (G0, G1, S, G2, and M) and their complex interplay with p53 and CDKs. Distinct cell cycle phases are demarcated by color-coded boxes, with detailed annotations highlighting ROS-mediated activation of specific signaling pathways and molecules (e.g., p53, CDKs, CKIs) to influence cell cycle progression or arrest. Examples include: G0 phase: ROS induces G0 arrest via activation of NRF2 and ATR/Chk1 signaling pathways. G1 phase: ROS triggers G1 arrest through PI3K/AKT and p53-dependent mechanisms. S phase: ROS promotes S phase arrest via ATM and p53-mediated pathways. G2 phase: ROS causes G2 arrest by activating WEE1/Myt1 and p53-related signaling. The schematic underscores ROS as a dual-functional modulator that orchestrates phase-specific cell cycle checkpoints through interactions with DNA damage sensors (e.g., ATM/ATR) and CDK inhibitors.
