Journal of Aging Research / 2011 / Article / Fig 2

Review Article

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

Figure 2

Altered Ca2+ signaling during aging and in age-related diseases. The Ca2+ dyshomeostasis during age is dependent on the cell type and the context. Most aged cells display decreased ER Ca2+ content and release, due to declined IP3R or RyR levels, reduced SERCA activity, and decreased Ca2+ buffering by intraluminal Ca2+-binding chaperones. However, in neurons and rat hearts, an enhanced Ca2+ signaling is found, caused by increasing IP3R or RyR activity. Age-related diseases (neurodegeneration, cardiac hypertrophy, and chronic heart failure) are also characterized by enhanced Ca2+ signaling. However, this property may be disease dependent, since a mouse model for Huntington’s disease displayed attenuated IP3R1 activity due to impaired binding of Grp78 to IP3R1. Hence, caution should be taken with general claims.
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