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Myopic defocus induction refers to the biological response to an optical condition where the focal plane of visual stimuli is set anterior (in front of) to the retina, typically induced by positive lenses or stimuli with a positive dioptric value[1][2][3]. This process is recognized by retinal cells—including glucagon amacrine cells[3]—within minutes, resulting in immediate changes (such as increased choroidal thickness) and longer-term changes like reduced axial elongation and modulation of gene expression related to metabolic and signaling pathways[1][2][3][6]. The response to myopic defocus is distinct from the response to hyperopic defocus (where the focal plane is behind the retina), as the retina uses separate molecular pathways to control eye growth bidirectionally (the Bidirectional Emmetropization by the Sign of Optical Defocus, BESOD model)[1][2]. Key signaling involved includes somatostatin receptor, Notch, JAK/STAT, dopamine, and integrin pathways, among others[1][2][6]. This physiological mechanism is not a molecule or drug target, but it is foundational to strategies designed to prevent myopic progression, such as multifocal lens designs or pharmaceutical modulation of retinal signaling[3][6]. Myopic defocus induction may be incorrectly listed as a molecular target due to its role in refractive development and its importance in myopia research, but it is best understood as an environmental stimulus or physiological process, not a receptor, enzyme, or canonical therapeutic target[1][2][3][6].
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