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Review ArticleReview Article

Endoplasmic Reticulum Ca2+ Handling in Excitable Cells in Health and Disease

Grace E. Stutzmann and Mark P. Mattson
David R. Sibley, ASSOCIATE EDITOR
Pharmacological Reviews September 2011, 63 (3) 700-727; DOI: https://doi.org/10.1124/pr.110.003814
Grace E. Stutzmann
Department of Neuroscience, Rosalind Franklin University/The Chicago Medical School, North Chicago, Illinois (G.E.S.); and Laboratory of Neurosciences, National Institute on Aging Intramural Research Program, Baltimore, Maryland (M.P.M.)
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Mark P. Mattson
Department of Neuroscience, Rosalind Franklin University/The Chicago Medical School, North Chicago, Illinois (G.E.S.); and Laboratory of Neurosciences, National Institute on Aging Intramural Research Program, Baltimore, Maryland (M.P.M.)
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David R. Sibley
Department of Neuroscience, Rosalind Franklin University/The Chicago Medical School, North Chicago, Illinois (G.E.S.); and Laboratory of Neurosciences, National Institute on Aging Intramural Research Program, Baltimore, Maryland (M.P.M.)
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Abstract

The endoplasmic reticulum (ER) is a morphologically and functionally diverse organelle capable of integrating multiple extracellular and internal signals and generating adaptive cellular responses. It plays fundamental roles in protein synthesis and folding and in cellular responses to metabolic and proteotoxic stress. In addition, the ER stores and releases Ca2+ in sophisticated scenarios that regulate a range of processes in excitable cells throughout the body, including muscle contraction and relaxation, endocrine regulation of metabolism, learning and memory, and cell death. One or more Ca2+ ATPases and two types of ER membrane Ca2+ channels (inositol trisphosphate and ryanodine receptors) are the major proteins involved in ER Ca2+ uptake and release, respectively. There are also direct and indirect interactions of ER Ca2+ stores with plasma membrane and mitochondrial Ca2+-regulating systems. Pharmacological agents that selectively modify ER Ca2+ release or uptake have enabled studies that revealed many different physiological roles for ER Ca2+ signaling. Several inherited diseases are caused by mutations in ER Ca2+-regulating proteins, and perturbed ER Ca2+ homeostasis is implicated in a range of acquired disorders. Preclinical investigations suggest a therapeutic potential for use of agents that target ER Ca2+ handling systems of excitable cells in disorders ranging from cardiac arrhythmias and skeletal muscle myopathies to Alzheimer disease.

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  • This article is available online at http://pharmrev.aspetjournals.org.

    doi:10.1124/pr.110.003814.

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Pharmacological Reviews: 63 (3)
Pharmacological Reviews
Vol. 63, Issue 3
1 Sep 2011
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Review ArticleReview Article

Endoplasmic Reticulum Ca2+ Handling in Excitable Cells in Health and Disease

Grace E. Stutzmann and Mark P. Mattson
Pharmacological Reviews September 1, 2011, 63 (3) 700-727; DOI: https://doi.org/10.1124/pr.110.003814

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Review ArticleReview Article

Endoplasmic Reticulum Ca2+ Handling in Excitable Cells in Health and Disease

Grace E. Stutzmann and Mark P. Mattson
Pharmacological Reviews September 1, 2011, 63 (3) 700-727; DOI: https://doi.org/10.1124/pr.110.003814
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  • Article
    • Abstract
    • I. Introduction
    • II. Endoplasmic Reticulum Ca2+ Homeostasis and Signaling
    • III. Pharmacology of Endoplasmic Reticulum Ca2+-Handling Systems
    • IV. Endoplasmic Reticulum Ca2+ within Specific Cells and Systems
    • V. Perturbed Endoplasmic Reticulum Ca2+ Handling and Disease
    • VI. Future Directions
    • Acknowledgments
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