## 4 Discussion
In this context, our findings add Myo/Nog cells to the growing list of retinal cell types capable of engaging in apoptotic clearance. Moreover, recent studies have proposed targeting phagocytosis-related receptors like BAII as a means to modulate neuroinflammatory outcomes in degenerative eye diseases [14]. These insights collectively suggest a broader and more cooperative network of phagocytic players in the retina than previously appreciated. The process of photoreceptor death in the rd1 model has been previously linked to apoptosis-inducing factor (AIF) translocation from the mitochondria to the nucleus, independent of caspase activation [11]. Recent studies have identified oxidative stress, particularly elevated hydrogen peroxide (H\({}_{2}\)O\({}_{2}\)), as a key upstream signal that promotes AIF-mediated cell death [11]. It is proposed that reactive oxygen species activate mitochondrial proteases, such as calpain 2, which cleave AIF and facilitate its nuclear translocation [27]. While this study did not directly assess oxidative stress markers, it is likely that H2O2 levels are elevated in the degenerating ONL [28], providing a potential explanation for the observed apoptosis and recruitment of phagocytic cells, including Myo/Nog cells. Interestingly, the spatial progression of photoreceptor degeneration in C3H mice revealed a more rapid decline at the retinal periphery compared to central regions, despite the relatively uniform rod and cone distribution in murine retinas [12]. This pattern differs from the peripheral rod-dominant degeneration observed in human RP [29]. While these differences underscore species-specific variations in retinal architecture, they also highlight the importance of studying regional degeneration dynamics to better understand disease progression and therapeutic targeting. Studies in the murine model of retinopathy of prematurity, ocular hypertension, acute brain injury, and retinal light damage indicate that Myo/Nog cells mitigate tissue damage [5; 6; 7; 16]. Applying such strategies to C3H/HeI mice could reveal whether their removal accelerates photoreceptor death or has an effect on inflammation. These experiments would provide direct evidence for their protective role in RP pathology. The therapeutic potential of Myo/Nog cells is particularly noteworthy. Previous studies have shown that the addition of brain-derived Myo/Nog cells mitigates neuronal cell death in models of ocular hypertension and retinal light damage, improving functional outcomes [5; 16]. In focal brain injury, supplementation with these cells reduced neuronal cell death [7]. Additionally, in a glaucoma model, Myo/Nog cell addition mitigated ganglion cell loss without altering intraocular pressure [6]. These studies collectively indicate that Myo/Nog cells are not merely passive responders but actively modulate neurodegenerative processes. In the context of retinitis pigmentosa, our current findings of Myo/Nog cell presence in degenerating retinal regions and their phagocytic activity suggest a similar modulatory role. In this study, the observation of endogenous Myo/Nog cells actively phagocytosing apoptotic photoreceptors suggests that augmenting their activity could further enhance retinal resilience. Leveraging Myo/Nog cell functions may offer a novel therapeutic strategy to slow the progression of RP. The genetic overexpression of BAII or the delivery of BAII agonists could enhance apoptotic debris clearance and neuroprotection. The transplantation of Myo/Nog cells, shown to preserve visual function in light-damage and brain injury models [7; 16], may be tested in RP models. Myo/Nog supplementation has the potential to enhance clearance as well as the delivery of neuroprotective molecules. The genetic alteration of BAII or targeting BAI1-mediated pathways and promoting Myo/Nog cell proliferation and migration to stressed regions are promising directions for future research.