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Journal of Aging Research
Volume 2011 (2011), Article ID 920178, 20 pages
Review Article

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

Laboratory 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, Belgium

Received 15 October 2010; Revised 23 December 2010; Accepted 5 January 2011

Academic Editor: Christiaan Leeuwenburgh

Copyright © 2011 Jean-Paul Decuypere et al. 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.


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.