Rb1, the retinoblastoma susceptibility gene, is a prototype tumor suppressor gene. It plays a crucial role in restraining cell cycle entry and, along with its family members, regulates numerous cellular processes and impacts cell response to various stimuli, ultimately determining cell fate [2,3,5]. Almost all mitogenic signals influence cell cycle progression by modulating the function of the RB1 protein through phosphorylation mediated by cyclin-CDK complexes [3].

In ischemic stroke, ginsenoside Rb1 inhibits astrocyte activation and promotes the transfer of astrocytic mitochondria to neurons. It does this by inhibiting NADH dehydrogenase in mitochondrial complex I, blocking reverse electron transport-derived ROS production, and thus inactivating astrocytes to protect mitochondria. In an ischemic mouse brain model, CD38 knockdown in the cerebral ventricles diminished the neuroprotective effects of ginsenoside Rb1, suggesting that astrocyte mitochondrial transfer is involved in the neuroprotective role of ginsenoside Rb1 [1]. In myocardial ischemia/reperfusion injury, ginsenoside Rb1 alleviates injury by inhibiting ROS production from mitochondrial complex I. It decreases mitochondrial ROS production, reduces myocardial infarct size, preserves cardiac function, and limits cardiac fibrosis [4].

In summary, Rb1 is a key tumor suppressor gene involved in cell cycle regulation. Studies using mouse models, such as those related to ischemic stroke and myocardial ischemia/reperfusion injury, have shown that ginsenoside Rb1, which may interact with Rb1-related pathways, can have protective effects through regulating mitochondrial-related processes. These findings contribute to understanding the role of Rb1-associated mechanisms in specific disease areas.