随着人工光的广泛使用和光电子产品的长期使用，光损伤（LD）对人类视网膜的影响已被确认为一种全球性威胁视力的问题。虽然有证据表明光引起的视网膜损伤与老年性黄斑变性导致的视力障碍之间存在显著相关性，但目前尚不清楚光诱导的视网膜退行性病变的表现方式以及是否有能够预防视网膜LD发展的药物。本研究探讨了蓝光导致光感受器细胞死亡的机制。通过观察视网膜器官样体和光感受器细胞对蓝光照射的反应，我们得出结论指出光感受器细胞可能发生显著的凋亡。我们证明了再生胰岛衍生1α（REG1A）能够通过增加抗凋亡基因Bcl2的表达和下调促凋亡基因Bax的表达，从而减少线粒体损伤，改善光感受器细胞的有氧能力，阻止其发生由LD引起的凋亡反应。REG1A首次被证明能够在LD引起的损伤后恢复线粒体功能并调节细胞凋亡，这表明其在预防和治疗视网膜视力损失方面具有潜在应用价值。© 2023年纽约科学院。

With the increased use of artificial light and the prolonged use of optoelectronic products, light damage (LD) to the human retina has been identified as a global vision-threatening problem. While there is evidence of a significant correlation between light-induced retinal damage and age-related vision impairment in age-related macular degeneration, it is unclear how light-induced retinal degeneration manifests itself and whether there are agents capable of preventing the development of LD in the retina. This study investigated a mechanism by which blue light leads to photoreceptor death. By observing blue light exposure in retinal organoids and photoreceptor cells, we concluded that there could be significant apoptosis of the photoreceptors. We demonstrate that regenerating islet-derived 1 alpha (REG1A) prevents photoreceptors from undergoing this LD-induced apoptosis by increasing expression of the anti-apoptotic gene Bcl2 and downregulating expression of the pro-apoptotic gene Bax, resulting in reduced mitochondrial damage and improved aerobic capacity in photoreceptor cells. For the first time, REG1A has been shown to restore mitochondrial function and cell apoptosis after LD-induced damage, suggesting its potential application in the prevention and treatment of retinal vision loss.© 2023 New York Academy of Sciences.