One in three people on Earth may need glasses for myopia within your lifetime — but glasses don't prevent the damage that high myopia causes. We're working on that.
Over the past three decades, myopia has become a epidemic in many countries. It is now predicted that 50% of the world’s population will be myopic by 2050 [PMID: 35059569] — a staggering public health challenge. Emmetropia is the condition in which the eye’s axial length matches its optical power, which leads to good visual acuity (absent astigmatism or other factors; Fig. 1). Myopia occurs when the emmetropic process fails and the eye grows excessively long, causing the focal plane to fall in front of the retina rather than on it. Although the refractive error can be corrected with glasses or contact lenses, high myopia substantially increases the risk of serious sight-threatening complications, including glaucoma, retinopathy, and retinal detachment [PMID: 31409941]. Effective interventions to slow or halt myopia progression therefore represent an urgent and largely unmet clinical need — one that requires a deeper understanding of the molecular signaling pathways that drive abnormal ocular growth (myopigenesis). Despite significant research efforts, these pathways remain incompletely characterized.
It is well established that refractive eye growth is modulated by visual input, which stimulates local retinal signaling and drives scleral extracellular matrix (ECM) remodeling — an obligate step in axial elongation. While several molecules are known to participate in myopigenic signaling, the precise mechanisms remain to be fully elucidated. A central focus of our lab is the role of all-trans retinoic acid (atRA) in myopigenesis. We have characterized atRA’s effects on the sclera [PMIDs: 37219510, 33468024] and investigated how atRA may be transported within the relevant ocular tissues [PMIDs: 40586643, 40987332]. We are actively pursuing these and related signaling pathways to build a more complete picture of what drives myopic eye growth.