Research Perspectives:

RIP Kinase-Mediated Necrosis as an Alternative Mechanism of Photoreceptor Death

Yusuke Murakami, Joan W. Miller and Demetrios G. Vavvas _

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Oncotarget. 2011; 2:497-509. https://doi.org/10.18632/oncotarget.286

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Yusuke Murakami, Joan W. Miller and Demetrios G. Vavvas

1Retina Service, Angiogenesis Laboratory, Department of Ophthalmology, Massachusetts Eye and Ear Infirmary, Harvard Medical School, Boston, Massachusetts, 02114, USA

Keywords: Photoreceptor, necroptosis, receptor interacting protein kinase

Received: June 2, 2011; Accepted: June 8, 2011; Published: June 10, 2011;


Demetrios G. Vavvas, e-mail:


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.

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