Mentor(s): Katia Del Rio-Tsonis

Retinal degeneration leads to irreversible vision loss and significantly impacts quality of life. Approximately 19.83 million Americans over the age of 40 are affected by age-related macular degeneration (AMD), a leading cause of retinal damage and vision loss (Rein et al., 2022). Current therapies can slow disease progression, but they do not fully restore lost retinal tissue or function (Khanani et al., 2023). Unlike humans, embryonic chickens possess a remarkable ability to regenerate their neural retina through two distinct mechanisms: activation of progenitor cells at the ciliary margin (CM) and reprogramming of the retinal pigment epithelium (RPE) (Luz-Madrigal et al., 2014; Wisely et al., 2017). Neural competence of RPE cells has also been demonstrated through induction of retinal fate genes such as Sox2 (Ma et al., 2009).


In this model, retina regeneration is restricted to embryonic day 4 (E4) and requires the presence of fibroblast growth factor 2 (FGF2) (Luz-Madrigal et al., 2014; Wisely et al., 2017). FGF2 binds to its receptor, the fibroblast growth factor receptor (FGFR), initiating intracellular signaling cascades that regulate cellular reprogramming. Previous work from our lab has demonstrated that FGFR signaling is essential for retina regeneration and RPE reprogramming (Spence et al., 2007). Additional studies have shown that regenerative responses in the chick retina are closely associated with signaling and metabolic state changes following injury (Echeverri-Ruiz et al., 2018).

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