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. Important during development and for the maintenance of homeostasis in some adult tissues, apoptosis is also associated with disease processes such as glaucoma.74 The goal of research in cell death mechanisms is to identify pharmacological means to protect retinal ganglion cells from degeneration regardless of the elevated IOP. Various approaches of pharmacological neuroprotection can be envisaged including supplying neurotrophic factors, inhibiting apoptosis, antagonizing excitotoxicity, and inhibiting the generation of neurotoxic molecules.71,75-81 A further approach might be boosting a protective, controlled autoimmune reaction.82 The clinical value of neuroprotective therapeutic strategies in human glaucoma needs still to be ascertained in clinical trials. However, an unquestionable prerequisite for such studies warrants adequate methods to evaluate progression of damage.83,84
A potential trigger for apoptotic retinal ganglion cell death in glaucoma could be an autoimmune reaction. Arguments in favor include the following: astrocytes, which express MHC class II antigens, may function as antigen-presenting cells;85 elevated serum antibodies against retinal heat shock proteins can be measured in glaucoma patients;86-88
expression of heat shock proteins is increased in neuronal and glial elements of the retina and optic nerve of glaucomatous eyes;89,90 exogenously applied heat shock proteins at concentrations similar to those found in glaucoma patients facilitate apoptotic cell death.91
