Apoptosis in ocular disease: a molecular overview
- 1 January 1996
- journal article
- review article
- Published by Taylor & Francis in Ophthalmic Genetics
- Vol. 17 (4) , 145-165
- https://doi.org/10.3109/13816819609057889
Abstract
Apoptosis is a form of genetically programmed cell death that can be induced by a variety of different stimuli. It is often referred to as a form of cellular suicide. Typically, apoptosis is characterized by the condensation and shrinkage of the cellular nucleus and cytoplasm, followed by the complete fragmentation of the cell and subsequent phagocytosis of the debris by surrounding cells. Although important during development, and also for maintaining homeostasis in some adult tissues, apoptosis can also be associated with disease processes. Recent laboratory studies indicate that apoptosis is a mechanism of cell death in several important ocular diseases including glaucoma, retinitis pigmentosa, cataract formation, retinoblastoma, retinal ischemia, and diabetic retinopathy. This review summarizes the results of these studies and provides a brief description of some of the key molecules that are involved in the genetic regulation of apoptosis. It is possible that a complete understanding of how these molecules function may someday lead to new treatment options aimed at blocking the death of cells in a variety of ocular diseases.Keywords
This publication has 102 references indexed in Scilit:
- Post-embryonic cell lineages of the nematode, Caenorhabditis elegansPublished by Elsevier ,2004
- Transcriptional or translational inhibition blocks low dose NMDA-mediated cell deathNeuroReport, 1995
- Greater sensitivity of larger retinal ganglion cells to NMDA-mediated cell deathNeuroReport, 1994
- Evidence supporting a role for programmed cell death in focal cerebral ischemia in rats.Stroke, 1993
- Internucleosomal DNA cleavage and neuronal cell survival/deathThe Journal of cell biology, 1993
- Mechanisms and Functions of Cell DeathAnnual Review of Cell Biology, 1991
- Aurintricarboxylic acid rescues PC12 cells and sympathetic neurons from cell death caused by nerve growth factor deprivation: correlation with suppression of endonuclease activity.The Journal of cell biology, 1991
- The Caenorhabditis elegans genes ced-3 and ced-4 act cell autonomously to cause programmed cell deathDevelopmental Biology, 1990
- Cloning the chromosomal breakpoint of t(14;18) human lymphomas: clustering around Jh on chromosome 14 and near a transcriptional unit on 18Cell, 1985
- Mutation and Cancer: Statistical Study of RetinoblastomaProceedings of the National Academy of Sciences, 1971