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Axial eye growth modulation refers to the regulation of the anteroposterior (axial) length of the eye, a key determinant of refractive errors such as myopia and hyperopia. This process is not controlled by a single receptor or enzyme but involves a complex interaction between visual environmental cues, the retina, choroid, and sclera, and numerous signaling pathways. Retinal cells (especially amacrine cells) synthesize and release molecules including dopamine, nitric oxide, acetylcholine, and neuropeptides, which, via multi-tissue signaling cascades, influence scleral remodeling and ocular growth rate[1]. Certain drugs that interact with muscarinic acetylcholine receptors, adenosine receptors, and alpha2-adrenoceptors have shown the ability to modulate these processes, offering therapeutic options for slowing myopic progression. Current evidence supports that "axial eye growth modulation" is a physiological output of multiple upstream targets and not a molecular entity itself; thus, it cannot be classified as a canonical molecular target[1][2][3][4].
Muscarinic acetylcholine receptor antagonism Adenosine receptor antagonism Alpha2-adrenoceptor agonism Nitric oxide signaling modulation
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