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Ocular growth refers to the complex physiological process of eye development and axial elongation, which is critical for achieving emmetropia, or normal vision [12, 13]. During development, the eye expands to match its optical power to its physical length; however, excessive growth leads to myopia (nearsightedness), where the eye becomes too long, causing light to focus in front of the retina [3, 4]. This process is governed by a signaling cascade initiated by visual stimuli in the retina, which is then relayed through the retinal pigment epithelium and choroid to the sclera, ultimately triggering extracellular matrix remodeling [4, 8, 11]. In pharmacological research, ocular growth is treated as a phenotypic target where the objective is to decelerate axial elongation to prevent high-myopia-related complications like retinal detachment [3, 9]. While not a single molecule, this process is clinically modulated by drugs targeting specific receptors, most notably muscarinic acetylcholine receptors and dopaminergic systems [1, 2, 8]. Current therapeutic strategies focus on stabilizing the axial length in pediatric populations to minimize long-term ocular morbidity [3, 11].
Drugs modulate ocular growth by targeting specific molecular receptors, such as muscarinic acetylcholine receptors or dopamine receptors, to inhibit scleral remodeling and decelerate axial elongation.
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