Opn3, also known as encephalopsin, is a member of the opsin family and a rhodopsin-like G-protein-coupled receptor (Rh-GPCR). It has diverse light-dependent and light-independent functions. It is widely expressed in various human tissues including the brain, eye, and skin-related cells. In the body, it may be involved in multiple biological processes such as angiogenesis, melanogenesis, and refractive development, and is associated with pathways like BRAFV600E/extracellular signal-regulated kinase, VEGFR2-AKT, and those related to autophagy and calcium-mediated signaling [1,4,5,6].

In Opn3 germline knockout mice, a refractive myopia phenotype was observed, which manifested in decreased lens thickness, shallower aqueous compartment depth, and shorter axial length. This indicates that Opn3 is required for normal refractive development and the GO/GROW response to induced myopia [2]. In zebrafish, knockdown or knockout of Opn3 impairs embryonic angiogenesis and vascular development. In human umbilical vein endothelial cells (HUVECs), silencing Opn3 inhibits cellular proliferation, migration, sprouting, and tube formation, while overexpression promotes these processes, suggesting its positive regulation of angiogenesis through the VEGFR2-AKT pathway [5].

In conclusion, Opn3 plays crucial roles in multiple biological processes. The gene knockout models in mice and zebrafish have revealed its importance in refractive development of the eye and angiogenesis. In addition, in melanocytic-related diseases, Opn3 has been shown to be involved in melanogenesis regulation and is associated with the prognosis of melanomas. These findings enhance our understanding of Opn3's functions and its potential as a therapeutic target in related diseases [1,2,3,5].