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[摘要]
调节功能异常(尤其是调节滞后)是介导近距离用眼与近视眼轴增长的核心枢纽。文章深入探讨了调节功能驱动眼轴延长的多维生物学机制:除经典的远视离焦信号诱发视网膜-脉络膜-巩膜生化重塑通路外,还存在睫状肌持续收缩对赤道部巩膜产生直接机械牵拉的生物力学通路,以及调节微波动异常导致视网膜成像质量下降而触发的异常生长通路。基于此综合机制,文章系统解析了药物(阿托品)、光学手段(角膜塑形镜、离焦镜)及视功能训练的防控原理。近视进展是光学离焦、机械应力及神经动态整合调控的综合结果,未来近视防控应基于个体的调节与遗传特征,走向精准、个性化的联合干预策略。
[Key word]
[Abstract]
Accommodative dysfunction, particularly accommodative lag, acts as a core hub connecting near work activity to myopic axial elongation. This review thoroughly explores the multidimensional biological mechanisms by which accommodative function drives axial growth. In addition to the classic pathway where hyperopic defocus signals induce retinal-choroidal-scleral biochemical remodeling, two other mechanisms are highlighted: a biomechanical pathway involving direct mechanical traction on the equatorial sclera caused by sustained ciliary muscle contraction, and a neural pathway where abnormal accommodative micro fluctuations degrade retinal image quality, thereby triggering abnormal ocular growth. Based on these comprehensive mechanisms, this paper systematically analyzes the principles of pharmacological(atropine), optical(orthokeratology, defocus lenses), and vision therapy interventions. Myopia progression results from the integrated regulation of optical defocus, mechanical stress, and neural dynamics. Future myopia control should advance toward precise, personalized combination strategies tailored to individual accommodative and genetic profiles.
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