IP3Receptors, Mitochondria, and Ca2+Signaling: Implications for Aging | Zendy

Jean-Paul Decuypere | Zendy; Giovanni Monaco | Zendy; Ludwig Missiaen | Zendy; Humbert De Smedt | Zendy; Jan B. Parys | Zendy; Geert Bultynck | Zendy

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IP₃Receptors, Mitochondria, and Ca²⁺Signaling: Implications for Aging

Author(s) -

Jean-Paul Decuypere,

Giovanni Monaco,

Ludwig Missiaen,

Humbert De Smedt,

Jan B. Parys,

Geert Bultynck

Publication year - 2011

Publication title -

journal of aging research

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 0.564

H-Index - 43

eISSN - 2090-2212

pISSN - 2090-2204

DOI - 10.4061/2011/920178

Subject(s) - autophagy , microbiology and biotechnology , endoplasmic reticulum , intracellular , mitochondrion , apoptosis , reactive oxygen species , signal transduction , oxidative stress , calcium signaling , homeostasis , biology , biochemistry

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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