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Significance Currently, there is no effective treatment for blindness resulting from loss of photoreceptors in humans. Elucidating degenerative pathways in photoreceptors may thus facilitate therapeutic strategies. Myocyte enhancer factor 2d (MEF2D) is a transcription factor known to be important for photoreceptor survival. Here, we explore the impact of low-level environmental light exposure on photoreceptor loss inMef2d -haploinsufficient mice. We elucidate a mechanism linking genes and environment, implicating oxidative stress in photoreceptor pathology. Specifically, we identify the MEF2D–nuclear factor (erythroid-derived 2)-like 2 (NRF2) pathway as a therapeutic target for photoreceptor survival. The transcription factor NRF2 stimulates antioxidant and antiinflammatory cascades. We find that activation of NRF2 with the pro-electrophilic drug carnosic acid can protectMef2d -haploinsufficient photoreceptors from light-induced damage.

MEF2D haploinsufficiency downregulates the NRF2 pathway and renders photoreceptors susceptible to light-induced oxidative stress