Apoptotic retinal ganglion cell loss is accompanied by complement and cytokine response in the βB1-CTGF primary open-angle glaucoma mouse model

Glaucoma is a multifactorial disease and occurs in many different species. In humans, glaucoma is accounted one of the leading causes for blindness worldwide. Due to glaucoma’s complexity, it is still unclear what pathomechanisms may be involved in its development in humans as well as in other species, such as canines. Diagnosis of glaucoma can be delayed because patients often do not notice a visual field loss until approximately 30% of retinal ganglion cells (RGCs) are lost (Kerrigan-Baumrind et al., 2000). Although the exact undergoing pathomechanisms of glaucoma disease are not fully understood yet, an increased intraocular pressure (IOP) is related to RGC death and is considered the main risk factor. To understand the underlying mechanisms more precisely, appropriate animal models are needed. For glaucoma research, many ocular hypertension models are available. In most of them, elevated IOP is introduced though surgical interventions, like injection of microbeads, laser coagulation, or cauterization of episcleral veins (Dey et al., 2018). Further, the most used genetic ocular hypertension model, the DBA2/J mouse, reflects more the secondary pigment dispersion glaucoma form rather than primary open-angle glaucoma (POAG; John et al., 1998). Hence, an ocular hypertension glaucoma model, which mimics POAG and does not need a surgical induction is of great interest for researchers.