IP3 Receptors, Mitochondria, and Ca2+ Signaling: Implications for Aging

The tight interplay between endoplasmic-reticulum-(ER-) and mitochondria-mediated Ca2+ signaling is a key determinant of cellular health and cellular fate through the control of apoptosis and autophagy. Proteins that prevent or promote apoptosis and autophagy can affect intracellular Ca2+ dynamics a...

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Main Authors: Jean-Paul Decuypere, Giovanni Monaco, Ludwig Missiaen, Humbert De Smedt, Jan B. Parys, Geert Bultynck
Format: Article
Language:English
Published: Wiley 2011-01-01
Series:Journal of Aging Research
Online Access:http://dx.doi.org/10.4061/2011/920178
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author Jean-Paul Decuypere
Giovanni Monaco
Ludwig Missiaen
Humbert De Smedt
Jan B. Parys
Geert Bultynck
author_facet Jean-Paul Decuypere
Giovanni Monaco
Ludwig Missiaen
Humbert De Smedt
Jan B. Parys
Geert Bultynck
author_sort Jean-Paul Decuypere
collection DOAJ
description The tight interplay between endoplasmic-reticulum-(ER-) and mitochondria-mediated Ca2+ signaling is a key determinant of cellular health and cellular fate through the control of apoptosis and autophagy. Proteins that prevent or promote apoptosis and autophagy can affect intracellular Ca2+ dynamics and homeostasis through binding and modulation of the intracellular Ca2+-release and Ca2+-uptake mechanisms. During aging, oxidative stress becomes an additional factor that affects ER and mitochondrial function and thus their role in Ca2+ signaling. Importantly, mitochondrial dysfunction and sustained mitochondrial damage are likely to underlie part of the aging process. In this paper, we will discuss the different mechanisms that control intracellular Ca2+ signaling with respect to apoptosis and autophagy and review how these processes are affected during aging through accumulation of reactive oxygen species.
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issn 2090-2212
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series Journal of Aging Research
spelling doaj-art-485b0c037a95447b8fedd8a7f3567bb72025-02-03T01:20:10ZengWileyJournal of Aging Research2090-22122011-01-01201110.4061/2011/920178920178IP3 Receptors, Mitochondria, and Ca2+ Signaling: Implications for AgingJean-Paul Decuypere0Giovanni Monaco1Ludwig Missiaen2Humbert De Smedt3Jan B. Parys4Geert Bultynck5Laboratory of Molecular and Cellular Signaling, Department of Molecular and Cellular Biology, K.U.Leuven, Campus Gasthuisberg O/N-1, Herestraat 49, Bus 802, 3000 Leuven, BelgiumLaboratory of Molecular and Cellular Signaling, Department of Molecular and Cellular Biology, K.U.Leuven, Campus Gasthuisberg O/N-1, Herestraat 49, Bus 802, 3000 Leuven, BelgiumLaboratory of Molecular and Cellular Signaling, Department of Molecular and Cellular Biology, K.U.Leuven, Campus Gasthuisberg O/N-1, Herestraat 49, Bus 802, 3000 Leuven, BelgiumLaboratory of Molecular and Cellular Signaling, Department of Molecular and Cellular Biology, K.U.Leuven, Campus Gasthuisberg O/N-1, Herestraat 49, Bus 802, 3000 Leuven, BelgiumLaboratory of Molecular and Cellular Signaling, Department of Molecular and Cellular Biology, K.U.Leuven, Campus Gasthuisberg O/N-1, Herestraat 49, Bus 802, 3000 Leuven, BelgiumLaboratory of Molecular and Cellular Signaling, Department of Molecular and Cellular Biology, K.U.Leuven, Campus Gasthuisberg O/N-1, Herestraat 49, Bus 802, 3000 Leuven, BelgiumThe tight interplay between endoplasmic-reticulum-(ER-) and mitochondria-mediated Ca2+ signaling is a key determinant of cellular health and cellular fate through the control of apoptosis and autophagy. Proteins that prevent or promote apoptosis and autophagy can affect intracellular Ca2+ dynamics and homeostasis through binding and modulation of the intracellular Ca2+-release and Ca2+-uptake mechanisms. During aging, oxidative stress becomes an additional factor that affects ER and mitochondrial function and thus their role in Ca2+ signaling. Importantly, mitochondrial dysfunction and sustained mitochondrial damage are likely to underlie part of the aging process. In this paper, we will discuss the different mechanisms that control intracellular Ca2+ signaling with respect to apoptosis and autophagy and review how these processes are affected during aging through accumulation of reactive oxygen species.http://dx.doi.org/10.4061/2011/920178
spellingShingle Jean-Paul Decuypere
Giovanni Monaco
Ludwig Missiaen
Humbert De Smedt
Jan B. Parys
Geert Bultynck
IP3 Receptors, Mitochondria, and Ca2+ Signaling: Implications for Aging
Journal of Aging Research
title IP3 Receptors, Mitochondria, and Ca2+ Signaling: Implications for Aging
title_full IP3 Receptors, Mitochondria, and Ca2+ Signaling: Implications for Aging
title_fullStr IP3 Receptors, Mitochondria, and Ca2+ Signaling: Implications for Aging
title_full_unstemmed IP3 Receptors, Mitochondria, and Ca2+ Signaling: Implications for Aging
title_short IP3 Receptors, Mitochondria, and Ca2+ Signaling: Implications for Aging
title_sort ip3 receptors mitochondria and ca2 signaling implications for aging
url http://dx.doi.org/10.4061/2011/920178
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