The Role of Calcium Stores in Apoptosis and Autophagy

Abstract

The mechanisms that regulate programmed cell death, such as apoptosis, and the cellular "self-eating" phenomenon of autophagy, share many regulatory systems and common pathways. These mechanisms have been extensively investigated over the last few years. Some intracellular structures may determine and control the autophagic fate of the cell such as the endoplasmic reticulum, mitochondria, and lysosomes. The coordination and interrelation of these organelles are crucial in maintaining calcium levels and general cellular homeostasis, as well as in regulating cell life and death under physiological and pathological conditions, including cancer, neurodegeneration, and aging. In this review, we discuss the crosstalk between the aforementioned organelles and their influence in apoptotic and autophagic processes.

Induction of apoptosis by UV in the flat oyster, Ostrea edulis

“…Stress of organelles including mitochondria, endoplasmic reticulum and lysosomes might lead to release of calcium into the cytoplasm. The increase of cytoplasmic calcium concentration is known to deregulate cells and induce apoptosis [50] as it has been shown in hemocytes of Penaeus monodon subjected to copper exposure [18]. Similarly, perturbation of DJm has been associated with apoptosis in invertebrates including Drosophila melanogaster and Lymnea stagnalis [8,51].…”

Aging of the auditory system

“…Thus, oxidative stress not only damages the mitochondrial membrane but also leads to a disturbed calcium regulation and hence to altered intracellular signal processes that entail disturbed cell metabolism and finally lead to cell death (Smaili et al, 2013).…”

“…Given the observation that all these parts of the stria vascularis, i.e., mitochondria, fibrocytes and endocholear potential, are reduced in ARHL, this suggests that a closely related and interdependent connection meticulously tunes the electrolyte exchange, particularly sodium, potassium, and calcium (Fig. 20.14) (Goto et al, 1999;Ichimiya et al, 2000;Wangemann, 2002;Spicer and Schulte, 2002;Ohlemiller et al, 2006;Mann et al, 2009;Smaili et al, 2013).…”

“…Calcium was shown on the one hand to have an important function in intracellular processes and cell signaling and on the other hand to be closely involved in genetics of aging (Takumida et al, 2009;Smaili et al, 2013). Furthermore, calcium not only provides the synaptic potential that permits a finely tuned signal transmission, but also has an important impact on neural viability and synaptic plasticity (Foster, 2007).…”

“…Contrariwise, age-related reduced calcium regulation alters mitochondrial activity that increases oxidative stress, leading to cell damage (Ouda et al, 2012;Smaili et al, 2013). Calcium dysregulation decreases neural transmission properties and leads to impaired or disrupted information exchange between the connected brain areas…”