视网膜变性中的坏死性凋亡与神经炎症
Necroptosis and Neuroinflammation in Retinal Degeneration.
作者信息
Tao Yan, Murakami Yusuke, Vavvas Demetrios G, Sonoda Koh-Hei
机构信息
Department of Ophthalmology, Graduate School of Medical Sciences, Kyushu University, Fukuoka, Japan.
Ines and Frederick Yeatts Retinal Research Laboratory, Retina Service, Department of Ophthalmology, Massachusetts Eye and Ear, Harvard Medical School, Boston, MA, United States.
出版信息
Front Neurosci. 2022 Jun 29;16:911430. doi: 10.3389/fnins.2022.911430. eCollection 2022.
Necroptosis mediates the chronic inflammatory phenotype in neurodegeneration. Receptor-interacting protein kinase (RIPK) plays a pivotal role in the induction of necroptosis in various cell types, including microglia, and it is implicated in diverse neurodegenerative diseases in the central nervous system and the retina. Targeting RIPK has been proven beneficial for alleviating both neuroinflammation and degeneration in basic/preclinical studies. In this review, we discuss the role of necroptosis in retinal degeneration, including (1) the molecular pathways involving RIPK, (2) RIPK-dependent microglial activation and necroptosis, and (3) the interactions between necroptosis and retinal neuroinflammation/degeneration. This review will contribute to a renewed focus on neuroinflammation induced by necroptosis and to the development of anti-RIPK drugs against retinal degeneration.
坏死性凋亡介导神经退行性变中的慢性炎症表型。受体相互作用蛋白激酶（RIPK）在包括小胶质细胞在内的多种细胞类型的坏死性凋亡诱导中起关键作用，并且它与中枢神经系统和视网膜中的多种神经退行性疾病有关。在基础/临床前研究中，靶向RIPK已被证明对减轻神经炎症和神经退行性变有益。在本综述中，我们讨论坏死性凋亡在视网膜变性中的作用，包括（1）涉及RIPK的分子途径，（2）RIPK依赖性小胶质细胞活化和坏死性凋亡，以及（3）坏死性凋亡与视网膜神经炎症/变性之间的相互作用。本综述将有助于重新关注由坏死性凋亡诱导的神经炎症，并有助于开发针对视网膜变性的抗RIPK药物。
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