Abstract
Age-related macular degeneration (AMD) is considered as the main worldwide cause of blindness in elderly adults. Exudative AMD type represents 10 to 15% of macular degeneration cases, but is the main cause of vision loss and blindness. Circadian rhythm changes are associated with aging and could further accelerate it. However, the link between circadian rhythms and exudative AMD is not fully understood. Some evidence suggests that dysregulation of circadian functions could be manifestations of diseases or could be risk factors for the development of disease in elderly adults. Biological rhythms are complex systems interacting with the environment and control several physiological pathways. Recent findings have shown that the dysregulation of circadian rhythms is correlated with exudative AMD. One of the main pathways involved in exudative AMD is the canonical WNT/β-catenin pathway. Circadian clocks have a main role in some tissues by driving the circadian expression of genes involved in physiological and metabolic functions. In exudative AMD, the increase of the canonical WNT/β-catenin pathway is enhanced by the dysregulation of circadian rhythms. Exudative AMD progression is associated with major metabolic reprogramming, initiated by aberrant WNT/β-catenin pathway, of aerobic glycolysis. This review focuses on the interest of circadian rhythm dysregulation in exudative AMD through the aberrant upregulation of the canonical WNT/β-catenin pathway.
Highlights
Age-related macular degeneration (AMD) is considered as the main worldwide cause of blindness in elderly adults [1]
Non-exudative AMD is marked by a progressive loss of the retinal pigment epithelium (RPE) cell layer and thinning of the retina, while exudative AMD is characterized by choroidal neovascularization (CNV) and sub-retinal neovascular fibrous tissue [2], leading to central vision deterioration [3]
Changes in energy metabolism are associated with metabolic and thermodynamic alterations and abnormal Circadian rhythm (CR) in exudative AMD
Summary
Age-related macular degeneration (AMD) is considered as the main worldwide cause of blindness in elderly adults [1]. The coordination and the modulation of CRs are organized by specific pacemaker structures, the primary circadian oscillations are controlled at the cell level. These oscillations are determined by numerous clock genes [22]. The input pathways generate a day-time to transpose it by the oscillators to the output pathways These output pathways control and regulate the expression of circadian clock genes to generate the rhythmicity. The output pathways are predicted to be rhythmic and controlled by the clock gene transcription factors These compounds, in turn, regulate downstream the circadian clock genes in a time-of-day-specific manner [27]. As in other mammals, melatonin is considered as an important influencer of CRs through its action on receptors in the nervous system [36]
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