Xiang Qin, Yang Jing, Liu Qing, Fang Jing, Li Xin, Fu Xinyu, Gao Xu, Fu Zhou
Department of Ophthalmology, Children's Hospital of Chongqing Medical University, National Clinical Research Center for Child Health and Disorders, Ministry of Education Key Laboratory of Child Development and Disorders, China International Science and Technology Cooperation base of Child development and Critical Disorders, Chongqing Key Laboratory of Pediatric Metabolism and Inflammatory Diseases, No. 136 Zhongshan Second Road, Yuzhong, Chongqing, China.
Department of Ophthalmology, Bishan Hospital of Chongqing Medical University, Bishan Hospital of Chongqing, Bishan, China.
Sci Rep. 2025 Aug 11;15(1):29392. doi: 10.1038/s41598-025-12800-2.
Myopia is the most widespread refractive error caused by an increase in the axial length (AL) of the eyeball, and is also a major risk factor for other blinding eye diseases, seriously endangering human health and quality of life. Investigating practical methods to control the progression of myopia is therefore crucial. The only medication that has been shown to effectively delay the progression of myopia over an extended period of time is atropine. Although they have more adverse effects, atropine eye drops with a high concentration work best to correct myopia. Atropine at low concentrations can slow the progression of myopia, however the results might not be very noticeable. It is of great significance to explore the application of drugs to suppress myopia in combination with low-concentration atropine in the treatment of myopia. This study investigated the role and mechanism of 0.01% atropine combined with carteolol hydrochloride in the treatment of myopia. By establishing a model of form-deprivation myopia in guinea pigs, we examined the protective effect of 0.01% atropine combined with carteolol hydrochloride on myopia in guinea pigs and further explored the mechanism of scleral remodeling mediated by mitochondrial dysfunction. We found that 0.01% atropine combined with carteolol hydrochloride refined mitochondrial dysfunction-induced extracellular matrix degradation by activating the PGC-1α/NRF2/HO-1 signaling pathway, thereby suppressing scleral remodeling and the progression of form-deprivation myopia in guinea pigs. In conclusion, 0.01% atropine combined with carteolol hydrochloride may be an effective strategy for the treatment of myopia.
近视是由眼球眼轴长度（AL）增加引起的最普遍的屈光不正，也是其他致盲性眼病的主要危险因素，严重危及人类健康和生活质量。因此，研究控制近视进展的实用方法至关重要。唯一被证明能在较长时间内有效延缓近视进展的药物是阿托品。虽然高浓度阿托品滴眼液副作用更多，但对矫正近视效果最佳。低浓度阿托品可减缓近视进展，不过效果可能不太明显。探索药物与低浓度阿托品联合应用在近视治疗中的作用具有重要意义。本研究探讨了0.01%阿托品联合盐酸卡替洛尔治疗近视的作用及机制。通过建立豚鼠形觉剥夺性近视模型，我们研究了0.01%阿托品联合盐酸卡替洛尔对豚鼠近视的保护作用，并进一步探讨了线粒体功能障碍介导的巩膜重塑机制。我们发现，0.01%阿托品联合盐酸卡替洛尔通过激活PGC-1α/NRF2/HO-1信号通路改善线粒体功能障碍诱导的细胞外基质降解，从而抑制豚鼠巩膜重塑和形觉剥夺性近视的进展。总之，0.01%阿托品联合盐酸卡替洛尔可能是治疗近视的有效策略。
