Abstract
1 Department of Epidemiology, Johns Hopkins Bloomberg School of Public Health, Baltimore, Maryland, United States of America, 2 Statistical Genetics Section, Inherited Disease Research Branch, National Human Genome Research Institute (NIH), Baltimore, Maryland, United States of America, 3 Department of Twin Research and Genetic Epidemiology, King’s College London School of Medicine, London, United Kingdom
Highlights
The etiology of myopia has been the subject of conjecture for centuries
The details of this mechanism are still emerging, its effect is to maintain homeostasis by adjusting eye growth so that the plane of the retina coincides with the focal point of the eye’s optical system, much like a camera lens focuses an image on its sensor
Kiefer and a group from 23andMe, Inc. [13] reported the results of the largest GWAS (n = 45,771) of a refractive phenotype conducted to date
Summary
Myopia (i.e., nearsightedness) is rapidly becoming a significant public health problem. The details of this mechanism are still emerging, its effect is to maintain homeostasis by adjusting eye growth so that the plane of the retina coincides with the focal point of the eye’s optical system, much like a camera lens focuses an image on its sensor In this paradigm, altered visual stimuli (e.g., optically blurred images) initiate a signaling cascade that originates locally in the sensory retina, traverses the retinal pigment epithelium and the vascular choroid, and regulates eye growth via active remodeling of the sclera—the rigid white connective tissue that forms the outer layer of the eye globe (Figure 1, panels A and B). Any gene that plays a role in this complex signaling pathway may contain susceptibility variants for myopia
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