Inhibition of PLK3 Attenuates Tubular Epithelial Cell Apoptosis after Renal Ischemia–Reperfusion Injury by Blocking the ATM/P53-Mediated DNA Damage Response

Figure 10

A schematic representation of the proposed mechanisms by which PLK3 regulates TEC apoptosis after DNA damage in response to oxidative stress. Renal I/R injury causes severe oxidative stress, and ROS attack double-stranded DNA, resulting in DSBs, which activate the ATM/PLK3/P53 signaling pathway in response to DNA damage, triggering the P53-dependent downstream apoptotic cascade, and thereby promoting TEC apoptosis.