Rb1, short for retinoblastoma susceptibility gene, is a prototype tumor suppressor gene. It plays a key role in restraining cell cycle entry and, along with its family members, regulates numerous cellular processes, determining cell fate. Its function is often suppressed through various mechanisms during tumor progression in many human cancers, such as prostate, lung, and breast cancer, and almost all familial and sporadic cases of retinoblastoma [2,4,5].

In ischemic stroke research, ginsenoside Rb1 (not to be confused with the Rb1 gene) inhibits astrocyte activation by blocking reverse electron transport-derived ROS production from mitochondrial complex I. It also promotes the transfer of astrocytic mitochondria to neurons, conferring neuroprotection. In a mouse model of brain ischemia, CD38 knockdown in the cerebral ventricles diminished the neuroprotective effects of ginsenoside Rb1, suggesting the role of astrocyte mitochondrial transfer in this process [1]. In myocardial ischemia/reperfusion injury studies, ginsenoside Rb1 alleviates injury in rats and protects H9C2 cells. It inhibits cardiomyocyte autophagy through the PI3K/Akt/mTOR signaling pathway, reducing the injury [3].

In summary, Rb1 is a crucial tumor suppressor gene, and its loss-of-function is associated with tumorigenesis in various cancers. Additionally, studies on ginsenoside Rb1 in animal models demonstrate its potential in protecting against ischemic stroke and myocardial ischemia/reperfusion injury, highlighting the importance of Rb1-related research in understanding disease mechanisms and potential therapeutic strategies.