Gas6, also known as growth arrest-specific gene 6, is a 75-kDa vitamin K-dependent protein. It belongs to the vitamin K-dependent family of proteins and is expressed in many human tissues. Gas6 regulates several biological processes in cells, such as proliferation, survival, and migration, by binding to its receptors Tyro3, Axl, and Mer (TAM) [6]. The Gas6/Axl signaling pathway is implicated in promoting cancer progression, metastasis, immune evasion, and therapeutic resistance [1]. Additionally, it is involved in processes like immune regulation, inflammation, and apoptotic cell clearance [2,3,4].

In septic mice, myocardial GAS6 levels decreased. GAS6 overexpression via adeno-associated virus 9 (AAV9) improved cardiac dysfunction, while GAS6 knockout removed these beneficial effects, revealing its role in sepsis-induced cardiac dysfunction through an NLRP3 inflammasome-dependent mechanism [2]. In the context of myocardial ischemia-reperfusion (IR) injury, GAS6, Axl, and SIRT1 levels were down-regulated in murine hearts and cardiomyocytes. GAS6 overexpression improved cardiac function, indicating its potential as a target for myocardial IR injury management [5].

In conclusion, Gas6 is crucial for multiple biological processes, especially in the context of diseases such as cancer, sepsis-induced cardiac dysfunction, and myocardial IR injury. Gene knockout models in mice have been instrumental in revealing its role in these disease conditions, highlighting its potential as a therapeutic target.