Acquired and inherited retinal disorders are responsible for vision loss in an increasing proportion of individuals worldwide. Photoreceptor (PR) death is central to the vision loss individuals experience in these various retinal diseases. Unfortunately, there is a lack of treatment options to prevent PR loss, so an urgent unmet need exists for therapies that improve PR survival and ultimately, vision. The retina is one of the most energy demanding tissues in the body, and this is driven in large part by the metabolic needs of PRs. Recent studies suggest that disruption of nutrient availability and regulation of cell metabolism may be a unifying mechanism in PR death. Understanding retinal cell metabolism and how it is altered in disease has been identified as a priority area of research. The focus of this review is on the recent advances in the understanding of PR metabolism and how it is critical to reduction-oxidation (redox) balance, the outer retinal metabolic ecosystem, and retinal disease. The importance of these metabolic processes is just beginning to be realized and unraveling the metabolic and redox pathways integral to PR health may identify novel targets for neuroprotective strategies that prevent blindness in the heterogenous group of retinal disorders.

获得性和遗传性视网膜疾病是导致全世界越来越多的人视力丧失的原因。光感受器 (PR) 死亡是个人在这些各种视网膜疾病中经历的视力丧失的核心。不幸的是，缺乏防止 PR 丢失的治疗选择，因此迫切需要改善 PR 存活率并最终改善视力的疗法。视网膜是身体中能量需求最高的组织之一，这在很大程度上是由 PR 的代谢需求驱动的。最近的研究表明，营养物质可用性的破坏和细胞代谢的调节可能是 PR 死亡的统一机制。了解视网膜细胞代谢及其在疾病中如何改变已被确定为优先研究领域。本综述的重点是对 PR 代谢及其对还原-氧化 (氧化还原) 平衡、外视网膜代谢生态系统和视网膜疾病的重要性的理解的最新进展。人们刚刚开始认识到这些代谢过程的重要性，阐明 PR 健康不可或缺的代谢和氧化还原途径可能会确定神经保护策略的新目标，以防止异质性视网膜疾病组失明。