Rod and cone photoreceptors degenerate in retinitis pigmentosa and age-related macular degeneration, robbing the visual system of light-triggered signals necessary for sight. However, changes in the retina do not stop with the photoreceptors. A stereotypical set of morphological and physiological changes, known as remodeling, occur in downstream retinal neurons. Some aspects of remodeling are homeostatic, with structural or functional changes compensating for partial loss of visual inputs. However, other aspects are nonhomeostatic, corrupting retinal information processing to obscure vision mediated naturally by surviving photoreceptors or artificially by vision-restoration technologies. In this review, I consider the mechanism of remodeling and its consequences for residual and restored visual function; discuss the role of retinoic acid, a critical molecular trigger of detrimental remodeling; and discuss strategies for suppressing retinoic acid biosynthesis or signaling as therapeutic possibilities for mitigating vision loss.

中文翻译：

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抑制视网膜重塑以减轻感光器退行性疾病中的视力丧失

视杆细胞和视锥细胞感光细胞在色素性视网膜炎和年龄相关性黄斑变性中退化，剥夺了视觉系统视力所需的光触发信号。然而，视网膜的变化并不仅仅限于光感受器。下游视网膜神经元中发生一组典型的形态和生理变化，称为重塑。重塑的某些方面是稳态的，结构或功能的变化可以补偿视觉输入的部分损失。然而，其他方面是非稳态的，会破坏视网膜信息处理，从而模糊由幸存的光感受器自然介导的视觉或由视觉恢复技术人为介导的视觉。在这篇综述中，我考虑了重塑的机制及其对残余和恢复视觉功能的影响；讨论视黄酸的作用，视黄酸是有害重塑的关键分子触发因素；并讨论抑制视黄酸生物合成或信号传导的策略作为减轻视力丧失的治疗可能性。