Retinal neuroprotection by growth factors: A mechanistic perspective

Retinal neuroprotection by growth factors: A mechanistic perspective For more than a decade it has been known that certain growth factors inhibit apoptosis in genetically determined and experimental models of inner and outer retinal degeneration. The molecular mechanisms underlying these protective effects and the signaling that supports the survival of photoreceptors and retinal ganglion cells in these models have recently come under more in depth investigation. This paper reviews our current understanding of the balance of pro‐ and antiapoptotic signals that determine cell fate in the retina and how the activation of key signal transduction pathways by specific classes of neurotrophins protects retinal neurons. © 2002 Wiley‐Liss, Inc. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Journal of Cellular Biochemistry Wiley

Retinal neuroprotection by growth factors: A mechanistic perspective

Journal of Cellular Biochemistry, Volume 88 (1) – Oct 31, 2002

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Publisher
Wiley
Copyright
Copyright © 2003 Wiley‐Liss, Inc., A Wiley Company
ISSN
0730-2312
eISSN
1097-4644
D.O.I.
10.1002/jcb.10354
Publisher site
See Article on Publisher Site

Abstract

For more than a decade it has been known that certain growth factors inhibit apoptosis in genetically determined and experimental models of inner and outer retinal degeneration. The molecular mechanisms underlying these protective effects and the signaling that supports the survival of photoreceptors and retinal ganglion cells in these models have recently come under more in depth investigation. This paper reviews our current understanding of the balance of pro‐ and antiapoptotic signals that determine cell fate in the retina and how the activation of key signal transduction pathways by specific classes of neurotrophins protects retinal neurons. © 2002 Wiley‐Liss, Inc.

Journal

Journal of Cellular BiochemistryWiley

Published: Oct 31, 2002

Keywords: apoptosis; growth factors; glaucoma; neuroprotection; photoreceptors; retina; retinal degeneration; retinal ganglion calls; signal transduction

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