本课题组新近通过对视黄醇脱氢酶13（RDH13）基因敲除鼠光损伤模型的研究发现，RDH13在视网膜光损伤中具有保护作用，同时体外研究发现RDH13具有视黄醛还原酶功能，能够还原对视网膜有光毒性作用的全反式视黄醛（atRAL），提示RDH13的这种保护作用可能与清除体内atRAL有关。贯序上述研究，以RDH13具有的视黄醛还原酶功能为思路，利用已建立的基因敲除鼠光损伤模型，探索RDH13通过调控atRAL代谢来保护视网膜抗atRAL毒性的机制；进一步通过检测atRAL介导的活性氧（ROS）及心磷脂（CL）参与的线粒体氧化应激损伤通路相关指标，观察RDH13功能缺失时细胞ROS变化及CL氧化情况，探讨RDH13是否通过抑制atRAL介导的线粒体氧化应激通路抗光损伤。通过上述研究旨在揭示RDH13对视网膜光损伤的保护机制，寻找有效的干预靶点，为视网膜光损伤新的防治方法提供科学依据。

Our current research on light-induced retinopathy in retinol dehydrogenase (RDH13) knockout (KO) mouse model reveals that RDH13 can protect the retina against light-induced retinopathy. Further observation shows that the RDH13 has the reductase function and can catalyze the reduction of light-related toxic all-trans-retinal (atRAL) in vitro. This implies that the mechanism of the protective effects may involve the clearance of vivo atRAL. Thus, based on the retinal reductase function of RDH13, we will use the already established RDH13 KO light damage model to explore whether RDH13 protects the retina against the toxicity of atRAL by regulating its metabolism. On the other hand, detecting the related indexes to observe the change of ROS and cardiolipin injury pathway so as to reveal the mechanism of RDH13 as a barrier protecting the retina against atRAL mediating ROS and cardiolipin involved mitochondrial oxidative stress damage. Based on the mechanism study, we aim to reveal the possible mechanism of the protective effects of RDH13 against light-induced retinopathy, find the effective target spots and provide the science evidence for the new treatment of light-induced retinopathy.