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Effects of Calcium Ion, Calpains, and Calcium Channel Blockers on Retinitis Pigmentosa

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 therapeu...

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Detalles Bibliográficos
Autor principal: Nakazawa, Mitsuru
Formato: Texto
Lenguaje:English
Publicado: Hindawi Publishing Corporation 2011
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3021879/
https://www.ncbi.nlm.nih.gov/pubmed/21253505
http://dx.doi.org/10.1155/2011/292040
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author Nakazawa, Mitsuru
author_facet Nakazawa, Mitsuru
author_sort Nakazawa, Mitsuru
collection PubMed
description 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.
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spelling pubmed-30218792011-01-20 Effects of Calcium Ion, Calpains, and Calcium Channel Blockers on Retinitis Pigmentosa Nakazawa, Mitsuru J Ophthalmol Review Article 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. Hindawi Publishing Corporation 2011 2010-12-23 /pmc/articles/PMC3021879/ /pubmed/21253505 http://dx.doi.org/10.1155/2011/292040 Text en Copyright © 2011 Mitsuru Nakazawa. https://creativecommons.org/licenses/by/3.0/ This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Review Article
Nakazawa, Mitsuru
Effects of Calcium Ion, Calpains, and Calcium Channel Blockers on Retinitis Pigmentosa
title Effects of Calcium Ion, Calpains, and Calcium Channel Blockers on Retinitis Pigmentosa
title_full Effects of Calcium Ion, Calpains, and Calcium Channel Blockers on Retinitis Pigmentosa
title_fullStr Effects of Calcium Ion, Calpains, and Calcium Channel Blockers on Retinitis Pigmentosa
title_full_unstemmed Effects of Calcium Ion, Calpains, and Calcium Channel Blockers on Retinitis Pigmentosa
title_short Effects of Calcium Ion, Calpains, and Calcium Channel Blockers on Retinitis Pigmentosa
title_sort effects of calcium ion, calpains, and calcium channel blockers on retinitis pigmentosa
topic Review Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3021879/
https://www.ncbi.nlm.nih.gov/pubmed/21253505
http://dx.doi.org/10.1155/2011/292040
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