Apoptosis, neuroprotection, and retinal ganglion cell death: An overview
Apoptosis, neuroprotection, and retinal ganglion cell death: An overview
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DOI:
10.1097/00004397-200101000-00011
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发表时间:
2001-12-01
影响因子:
--
通讯作者:
Grosskreutz, CL
中科院分区:
文献类型:
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作者:
Farkas, RH;Grosskreutz, CL
Retinal ganglion cell death, clinically recognized as optic neuropathy, is a common cause of vision loss for which current treatments are often inadequate. Glaucoma, by far the most common optic neuropathy, can be slowed by lowering intraocular pressure but often progresses despite such efforts. Fewer treatment options exist for most other causes of ganglion cell death, such as trauma or optic neuritis. Over recent years, two important concepts have emerged about the way cells die. The first is that most, if not all, mammalian cells can die through complex, active cellular processes rather than simply from a passive loss of homeostasis. Such active cellular death has been termed apoptosis. The second concept is that even though a seemingly infinite variety of insults can kill cells, many of the most common act through similar final common pathways. There is great hope that novel treatment strategies for diseases ranging from neurodegeneration to cancer might arise from modulating apoptosis and the final common pathways that lead to it. This hope extends to ophthalmic diseases as well. 1–6 To understand the therapeutic promise of neuroprotection and modulation of apoptosis, one must begin by briefly reexamining our basic understanding of these processes. With the recent explosion of knowledge about cell death, the terms themselves have taken on a largerthan-life aura, and even the most basic definitions continue to evolve.