Ca<sup>2+</sup>in quality control

East, Daniel A.; Campanella, Michelangelo

doi:10.4161/auto.25367

Cited by 94 publications

(39 citation statements)

References 102 publications

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“…When cells encounter stressful situations, they can either try to survive under these conditions via a very beneficial process called autophagy, or by activating a programmed cell death program through the process of apoptosis [11, 18, 20]. The word autophagy is derived from the Greek roots “auto” (self) and “phagy” (eating) and broadly refers to the cellular catabolic processes in which target material is transported to lysosomes for degradation.…”

Section: Autophagymentioning

confidence: 99%

“…Since then the mechanism by which Ca 2+ controls the autophagy remains controversial [18]. Previous studies have shown an inhibitory action of Ca 2+ on autophagy [11, 31] while many recent studies showed a positive role of Ca 2+ that activate autophagy [18, 34-36]. The majority of studies showing Ca 2+ permeable channels as autophagy regulators are focused on the inositol trisphosphate receptor (IP 3 R) which is the main intracellular Ca 2+ release channel [37].…”

Section: Autophagymentioning

confidence: 99%

“…Modulation of Ca 2+ permeable channels expression/function also affects intracellular Ca 2+ concentrations and consequently Ca 2+ dependent processes, such as cell proliferation, ER stress, apoptosis, and autophagy [1, 10, 11]. Ca 2+ permeable channels, including families of transient receptor potential (TRP) channels, Orai's, voltage-gated Ca 2+ channels, two-pore Ca 2+ channels, mitochondrial Ca 2+ uniporter, IP 3 and ryanodine receptors have all been identified to contribute towards changes in intracellular Ca 2+ ([Ca 2+ ] i ) [7, 8, 12, 13].…”

Section: Introductionmentioning

confidence: 99%

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Functional role of TRP channels in modulating ER stress and Autophagy

et al. 2016

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Intracellular calcium (Ca2+) levels play a vital role in regulating cellular fate. The coordination and interrelation among the cellular organelles, mainly the intracellular Ca2+ stores in endoplasmic reticulum (ER), are crucial in maintaining cytosolic Ca2+ levels and in general cellular homeostasis. Moreover, maintaining Ca2+ homeostasis is essential for regulating diverse and sometimes opposing processes such as cell survival and cell death in disease conditions such as, neurodegeneration, cancer and aging. Ca2+ is able to regulate opposing functions by either regulating the cellular “self-eating” phenomenon of autophagy to promote cell survival or by regulating the programmed cell death process of apoptosis. Autophagy is also important for cell survival especially after induction of ER stress and association between ER stress and autophagy may have relevance to numerous diseases. Moreover, a multitude of evidence is emerging that the functional regulation of TRP channels, their unique localization, and their interaction with other Ca2+-sensing elements define these diverse regulatory pathways. It is this unique function which allows individual TRP channels to contribute differently in the regulation of cell fate and, in turn, determines the precise effect of modulating Ca2+ signaling via the particular channel. Thus, in this review we have focused on the aspects of TRP channel localization and function (Ca2+ signaling) that affects the ER stress and autophagic process.

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Section: Autophagymentioning

confidence: 99%

Section: Autophagymentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Functional role of TRP channels in modulating ER stress and Autophagy

et al. 2016

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“…CAMKKβ can activate AMPK which initiates autophagy by multiple mechanisms. Other studies suggested that Ca 2+ -induced autophagy through protein kinase C theta or ERK1/2 [52]. Future research is needed to identify the mechanisms by which elevated cytosolic Ca 2+ can induce or inhibit autophagy in different conditions and cell types.…”

Section: Signaling Molecules Downstream Of Gpcrs That Regulate Autophagymentioning

confidence: 99%

G protein-coupled receptors and the regulation of autophagy

Wauson

Dbouk

Ghosh

et al. 2014

Trends in Endocrinology & Metabolism

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Autophagy is an important catabolic cellular process that eliminates damaged and unnecessary cytoplasmic proteins and organelles. Basal autophagy occurs during normal physiological conditions, but the activity of this process can be significantly altered in human diseases. Thus, defining the regulatory inputs and signals that control autophagy is essential. Nutrients are key modulators of autophagy. While autophagy is generally accepted to be regulated in a cell autonomous fashion, recent studies suggest nutrients can modulate autophagy in a systemic manner by inducing the secretion of hormones and neurotransmitters that regulate G protein-coupled receptors (GPCRs). Emerging studies show that GPCRs also regulate autophagy by directly detecting extracellular nutrients. We review the role of GPCRs in autophagy regulation, highlighting their potential as therapeutic drug targets.

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“…Mitochondria are also central to several other processes in cellular homeostasis. The ability to buffer cytosolic calcium (Ca 2+ ), is fundamental in shaping cellular Ca 2+ signals (East and Campanella, 2013), and reactive oxygen species (ROS) generated as a by-product of respiration act as both signalling molecules and a major source of oxidative stress (Duchen and Szabadkai, 2010).…”

Section: Introductionmentioning

confidence: 99%