摘要近视是公共卫生领域的重要问题。低强度红光治疗以其非侵入性的方式，已被证实可有效延缓眼轴增长，但其机制尚不明确。低强度红光治疗基于特定分子吸收光子并响应光信号的原理，导致分子电子激发态改变，暂时性地改变其结构和功能，实现高特异性和靶向的生物调节。眼轴长度的调节涉及复杂的级联反应，起始于视网膜并影响巩膜。光暴露与眼轴增长密切相关。研究表明，低强度红光引起的视觉刺激由视网膜神经元接收并产生信号经视网膜色素上皮和脉络膜转导至巩膜，引起神经递质释放、脉络膜血流改变和巩膜重塑。本文综述了低强度红光治疗与眼轴调节的关系以及低强度红光延缓眼轴增长的相关机制。( 国际眼科纵览，2024, 48：426－432)

abstractsMyopia has become an urgent problem in global public health. Low-intensity red light therapy has been shown to be effective in delaying axial elongation in a non-invasive manner, but its mechanism remains unclear. Low-intensity red light therapy is based on the principle that specific molecules absorb photons and respond to light signals, resulting in changes in the electronic excited state of molecules, temporarily changing their structure and function, and achieving highly specific and targeted biological regulation. The regulation of axial length involves a complex cascade of reactions that begins in the retina and affects the sclera. Light exposure is closely related to axial elongation. Previous studies have indicated that the visual stimulation elicited by low-intensity red light is received by retinal neurons and generates signals, which are transduced through the retinal pigment epithelium and choroid to the sclera, leading to the release of neurotransmitters, alterations in choroidal blood flow, and scleral remodeling. This review explores the relationship between low-intensity red light therapy and axial regulation, investigating the mechanisms by which low-intensity red light slows down axial growth. ( Int Rev Ophthalmol, 2024, 48: 426-432)