The Wilmer Eye Institute, Johns Hopkins University, School of Medicine, Baltimore, MD, USA.
Adv Exp Med Biol. 2018;1074:351-357. doi: 10.1007/978-3-319-75402-4_43.
c-Jun N-terminal kinase (JNK), a member of stress-induced mitogen-activated protein (MAP) kinase family, has been shown to modulate a variety of biological processes associated with neurodegenerative pathology of the retina. In particular, various retinal cell culture and animal models related to glaucoma, age-related macular degeneration (AMD), and retinitis pigmentosa indicate that JNK signaling may contribute to disease pathogenesis. This mini-review discusses the impact of JNK signaling in retinal disease, with a focus on retinal ganglion cells (RGCs), photoreceptor cells, retinal pigment epithelial (RPE) cells, and animal studies, with particular attention to modulation of JNK signaling as a potential therapeutic target for the treatment of retinal disease.
c-Jun N-末端激酶（JNK）是应激诱导的丝裂原活化蛋白（MAP）激酶家族的成员，已被证明可调节与视网膜神经退行性病变相关的多种生物学过程。特别是与青光眼、年龄相关性黄斑变性（AMD）和视网膜色素变性相关的各种视网膜细胞培养和动物模型表明，JNK 信号可能有助于疾病的发病机制。本综述讨论了 JNK 信号在视网膜疾病中的作用，重点关注视网膜神经节细胞（RGC）、光感受器细胞、视网膜色素上皮（RPE）细胞以及动物研究，并特别关注 JNK 信号的调节作为治疗视网膜疾病的潜在治疗靶点。
