Murakami Yusuke, Miller Joan W, Vavvas Demetrios G
Retina Service, Angiogenesis Laboratory, Department of Ophthalmology, Massachusetts Eye and Ear Infirmary, Harvard Medical School, Boston, Massachusetts 02114, USA.
Oncotarget. 2011 Jun;2(6):497-509. doi: 10.18632/oncotarget.286.
Photoreceptor cell death is the terminal event in a variety of retinal disorders including age-related macular degeneration, retinitis pigmentosa, and retinal detachment. Apoptosis has been thought to be the major form of cell death in these diseases, however accumulating evidence suggests that another pathway, programmed necrosis is also important. Recent studies have shown that, when caspase pathways are blocked, receptor interacting protein (RIP) kinases promote necrosis and overcome apoptosis inhibition. Therefore, targeting of both caspase and RIP kinase pathways are required for effective photoreceptor protection. Here, we summarize the current knowledge of RIP kinase-mediated necrotic signaling and its contribution to photoreceptor death.
光感受器细胞死亡是多种视网膜疾病的终末事件,包括年龄相关性黄斑变性、视网膜色素变性和视网膜脱离。凋亡一直被认为是这些疾病中细胞死亡的主要形式,然而越来越多的证据表明,另一条途径——程序性坏死也很重要。最近的研究表明,当半胱天冬酶途径被阻断时,受体相互作用蛋白(RIP)激酶会促进坏死并克服凋亡抑制。因此,有效的光感受器保护需要同时靶向半胱天冬酶和RIP激酶途径。在此,我们总结了目前关于RIP激酶介导的坏死信号及其对光感受器死亡的作用的认识。