Abstract
Recent advances in molecular genetic studies have revealed many of the causative genes of retinitis pigmentosa (RP). These achievements have provided clues to the mechanisms of photoreceptor degeneration in RP. Apoptosis is known to be a final common pathway in RP and, therefore, a possible therapeutic target for photoreceptor rescue. However, apoptosis is not a single molecular cascade, but consists of many different reactions such as caspase-dependent and caspase-independent pathways commonly leading to DNA fractionation and cell death. The intracellular concentration of calcium ions is also known to increase in apoptosis. These findings suggest that calpains, one of the calcium-dependent proteinases, play some roles in the process of photoreceptor apoptosis and that calcium channel antagonists may potentially inhibit photoreceptor apoptosis. Herein, the effects of calpains and calcium channel antagonists on photoreceptor degeneration are reviewed.
Highlights
Retinitis pigmentosa (RP) represents a group of hereditary retinal degenerations principally characterized by progressive rod-dominant photoreceptor degeneration in the initial stage and eventual cone photoreceptor degeneration in later stages
Molecular genetic studies have demonstrated that a primary lesion in RP involves photoreceptor and/or retinal pigment epithelial cells in which many causative genes are expressed under physiological conditions
This paper mainly focuses on studies examining the effects of calcium ions and calpains on photoreceptor apoptosis, as well as pharmacological treatments for RP using calcium channel antagonists
Summary
Retinitis pigmentosa (RP) represents a group of hereditary retinal degenerations principally characterized by progressive rod-dominant photoreceptor degeneration in the initial stage and eventual cone photoreceptor degeneration in later stages. Heredities are heterogeneous, characterized by at least 3 different modes of inheritance, such as autosomaldominant, autosomal-recessive, and X-linked patterns. Molecular genetic studies have demonstrated that a primary lesion in RP involves photoreceptor and/or retinal pigment epithelial cells in which many causative genes are expressed under physiological conditions. Photoreceptor or retinal pigment epithelial cells are known to degenerate mostly through apoptosis [2], which is understood as a final common pathway for RP at the cellular level. As the mechanisms of photoreceptor degeneration have been gradually elucidated, studies on therapeutic approaches have dramatically increased, including pharmacotherapy, cellular transplantation, gene therapy, regenerative therapy, and retinal prosthesis. This paper mainly focuses on studies examining the effects of calcium ions and calpains on photoreceptor apoptosis, as well as pharmacological treatments for RP using calcium channel antagonists
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