Photoreceptor cell death and rescue in retinal detachment and degenerations

Yusuke Murakami, Shoji Notomi, Toshio Hisatomi, Toru Nakazawa, Tatsuro Ishibashi, Joan W. Miller, Demetrios G. Vavvas

研究成果: ジャーナルへの寄稿総説査読

142 被引用数 (Scopus)

抄録

Photoreceptor cell death is the ultimate cause of vision loss in various retinal disorders, including retinal detachment (RD). Photoreceptor cell death has been thought to occur mainly through apoptosis, which is the most characterized form of programmed cell death. The caspase family of cysteine proteases plays a central role for inducing apoptosis, and in experimental models of RD, dying photoreceptor cells exhibit caspase activation; however, there is a paradox that caspase inhibition alone does not provide a sufficient protection against photoreceptor cell loss, suggesting that other mechanisms of cell death are involved. Recent accumulating evidence demonstrates that non-apoptotic forms of cell death, such as autophagy and necrosis, are also regulated by specific molecular machinery, such as those mediated by autophagy-related proteins and receptor-interacting protein kinases, respectively. Here we summarize the current knowledge of cell death signaling and its roles in photoreceptor cell death after RD and other retinal degenerative diseases. A body of studies indicate that not only apoptotic but also autophagic and necrotic signaling are involved in photoreceptor cell death, and that combined targeting of these pathways may be an effective neuroprotective strategy for retinal diseases associated with photoreceptor cell loss.

本文言語英語
ページ(範囲)114-140
ページ数27
ジャーナルProgress in Retinal and Eye Research
37
DOI
出版ステータス出版済み - 11月 2013

!!!All Science Journal Classification (ASJC) codes

  • 眼科学
  • 感覚系

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