Future Directions 

Our future research will focus on analyzing other signaling pathways downstream of FGF2-FGFR interactions that govern RPE reprogramming. We hypothesize that FGF2-induced RPE reprogramming proceeds without essential involvement of the MAPK pathway. To test this hypothesis, we will use pharmacological inhibitors specifically targeting Src-family kinases, JNK, and PKC downstream signaling cascades. Also, we will continue to test the PI3K/AKT pathway with the LY294002 inhibitor for further confirmation that this interaction does not prevent the reprogramming of RPE cells. These experiments will be conducted in the RPE explant model, which closely mirrors the molecular and cellular events of in vivo retina regeneration driven by RPE reprogramming. 

By pinpointing the exact pathways required for efficient reprogramming, we aim to identify molecular targets that could be leveraged for therapeutic purposes in human retinal degenerative diseases, such as age-related macular degeneration and retinitis pigmentosa. Ultimately, understanding the signaling networks that drive RPE-to-retina conversion may inform the development of novel treatment options, ranging from small-molecule modulators to cell replacement strategies, that restore or preserve vision in patients suffering from retinal disorders.