Myopia is the most common eye disorder in the world which is caused by a mismatch between the optical power of the eye and its excessively long axial length. Recent studies revealed that the regulation of the axial length of the eye occurs via a complex signaling cascade, which originates in the retina and propagates across all ocular tissues to the sclera. The complexity of this regulatory cascade has made it particularly difficult to develop effective antimyopia drugs. The current pharmacological treatment options for myopia are limited to atropine and 7-methylxanthine, which have either significant adverse effects or low efficacy. In this review, we focus on the recent advances in genome-wide studies of the signaling pathways underlying myopia development and discuss the potential of systems genetics and pharmacogenomic approaches for the development of antimyopia drugs.

中文翻译：

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抗近视药物开发的药物基因组学方法：路径引领。

近视是世界上最常见的眼部疾病，它是由眼睛的屈光力与其过长的眼轴长度不匹配引起的。最近的研究表明，眼睛轴向长度的调节是通过复杂的信号级联反应发生的，该级联反应起源于视网膜并通过所有眼部组织传播到巩膜。这种监管级联的复杂性使得开发有效的抗近视药物变得特别困难。目前近视的药物治疗选择仅限于阿托品和 7-甲基黄嘌呤，它们要么具有显着的不良反应，要么疗效低。在这次审查中，