Other studies have found that in chronic stress-induced depression models, knockout of uncoupling protein 2 (UCP2) leads to mitochondrial dysfunction, abnormal mitochondrial membrane potential, and overload of the electron transport chain, resulting in ROS accumulation and oxidative stress [70,71], promoting the activation of the ROS-TXNIP-NLRP3 inflammasome axis, which causes the release of pro-inflammatory factors such as IL-1β, leading to impaired neurogenesis, loss of astrocytes, and mitochondrial energy metabolism disorders, ultimately mediating the onset of depression [72]. The gene discussed is IL1B; the disease is depressive symptom measurement.