Angpt4, also known as Ang3, is a significant regulator in multiple biological processes. It is a ligand for endothelial receptor tyrosine kinase Tie2 and plays crucial roles in endothelial cell proliferation, survival, angiogenesis, and fluid homeostasis [3,4]. Angpt4 affects important signaling pathways such as ERK1/2 and PI3K/AKT downstream of TIE2, which are involved in various physiological and pathological events [1,2]. Genetic models, including mouse models, have been instrumental in studying its functions.

In mice, deletion of Angpt4 combined with Angpt2 deletion led to detrimental effects on Schlemm's canal morphology, resulting in glaucomatous changes, indicating an additive effect of Angpt4 in Schlemm's canal maintenance and Tie2 activation [3]. In the retina, Angpt4 deletion caused defective venous development, impaired venous drainage, and neuronal cell defects, identifying it as essential for venous-specific development, remodeling, retinal fluid clearance, and neuronal function [4].

In conclusion, Angpt4 is vital for maintaining the integrity of structures like Schlemm's canal and the retina. Mouse models with Angpt4 gene knockout or combined knockout with other related genes have revealed its role in diseases such as glaucoma and in maintaining retinal function. These findings contribute to understanding the mechanisms of related diseases and may provide potential therapeutic targets.