Myopia, or short-sightedness, usually develops when the eye grows too long, causing distant images to be focused in front of the retina. Although vision can generally be corrected with glasses or contact lenses, myopia is not a harmless condition. It increases the lifetime risk of retinal detachment, glaucoma, cataract and myopic macular degeneration, all of which can lead to permanent visual impairment. Its prevalence is rising rapidly: approximately 23% of the global population was affected in 2000, and this proportion is projected to reach around 50% by 2050. The associated global economic burden has also been estimated to rise substantially, reflecting healthcare costs, loss of productivity and the effect of visual impairment on quality of life.
Both genetic and environmental factors influence myopia. Insufficient time outdoors and prolonged near work are recognised risk factors, but growing evidence also points to a relationship with sleep and circadian rhythms, the internal biological processes that organise daily patterns of behaviour and physiology. Children with myopia have been reported to have later and more irregular sleep schedules, while genetic variants associated with refractive errors are enriched near genes involved in molecular clock regulation. Previous human analyses underlying CHRONOPIA also identified associations between chronotype, social jet lag, sleep duration and refractive errors. However, observational associations alone cannot establish whether altered circadian timing contributes to abnormal eye growth, whether refractive errors themselves disturb retinal rhythms, or whether both arise through shared biological mechanisms.
CHRONOPIA addresses these gaps by investigating the relationship between circadian rhythms and myopia from several complementary perspectives. First, it examines whether changing environmental light-dark timing alters refractive development and susceptibility to myopia. Second, it investigates how experimentally induced myopia affects daily molecular rhythms and gene expression in the retina. Third, it compares genes and biological pathways identified in mouse models with human genetic findings to determine which mechanisms may be shared across species and therefore most relevant to human myopia.
The project combines controlled animal experiments, ocular imaging, retinal RNA sequencing, circadian biology, bioinformatics and human genetics. This interdisciplinary approach links experimental evidence about causality and biological mechanisms with population-level human data. In the longer term, the results are expected to improve understanding of how environmental light timing, retinal biology and genetic susceptibility interact in myopia. They may also improve the design and interpretation of experimental models, support the identification of candidate molecular targets and provide a stronger evidence base for future prevention and treatment research. Because even a modest reduction in the prevalence or progression of myopia could reduce visual impairment and its economic and societal burden, the project has potential relevance for researchers, eye-care professionals and public-health stakeholders.
