Intracellular Ca2+ signaling and Ca2+ microdomains in the control of cell survival, apoptosis and autophagy. Issue 2 (August 2016)

• Record Type: Journal Article
• Authors: La Rovere, Rita M.L.; Roest, Gemma; Bultynck, Geert; Parys, Jan B.
• Is Part Of: Cell calcium. Volume 60:Issue 2(2016)
• Page Start: 74
• Page End: 87
• Publication Date: 2016-08
• Subjects: Apoptosis -- Autophagy -- Endoplasmic reticulum -- IP3 receptor -- Lysosomes -- Mitochondria; AMBRA1 autophagy/Beclin 1 regulator 1 -- AMPK AMP-activated kinase -- ATF4 activating transcription factor-4 -- Atg autophagy-related -- BIRD-2 Bcl-2/IP3R disruptor-2 -- CREB cAMP response element-binding protein -- ER endoplasmic reticulum -- ERMES ER mitochondria encounter structure -- ETC electron-transport chain -- GRP75 glucose-regulated protein 75 -- GSK3β glycogen synthase kinase-3β -- IDH isocitrate dehydrogenase -- IP3 inositol 1, 4, 5-trisphosphate -- IP3R IP3 receptor -- αKGDH α-ketoglutarate dehydrogenase -- LC3 microtubule-associated protein light chain 3 -- LRRK2 leucine-rich repeat kinase 2 -- MAM mitochondria-associated membrane -- MCU mitochondrial Ca2+ uniporter -- MEF mouse embryonic fibroblast -- Mfn mitofusin -- mPTP mitochondrial permeabilization transition pore -- mTORC1 mammalian or mechanistic target of rapamycin complex 1 -- NAADP nicotinic acid adenine dinucleotide phosphate -- NFAT nuclear factor of activated T cells -- PDH pyruvate dehydrogenase -- PERK protein kinase RNA-like ER kinase -- PML promyelocytic leukemia -- PTEN phosphatase and tensin homolog -- ROS reactive oxygen species -- RyR ryanodine receptor -- SDH succinate dehydrogenase -- SERCA sarco-/endoplasmic Ca2+-ATPase -- TCA tricarboxylic acid -- TFEB transcription factor EB -- TMBIM transmembrane Bax inhibitor motif -- TPC2 two-pore channel 2 -- TRP transient receptor potential -- ULK1/2 Atg1/Unc-51-like kinase 1/2 -- UPR unfolded protein response -- VDAC voltage-dependent anion channel; Calcium -- Metabolism -- Periodicals; Vertebrates -- Physiology -- Periodicals; Calcium -- Physiological effect -- Periodicals; Cell physiology -- Periodicals; Calcium in the body -- Periodicals; 572.516
• DOI: 10.1016/j.ceca.2016.04.005
• Languages: English
• ISSNs: 0143-4160

Abstract

Graphical abstract: Highlights: Various Ca 2+ microdomains exist in living cells. Basal Ca 2+ transfer between ER and mitochondria enhances cellular bioenergetics. Excessive Ca 2+ transfer between ER and mitochondria induces apoptosis. Ca 2+ release from the ER and from the lysosomes regulates autophagy. Ca 2+ microdomains critically control cell survival and cell death decisions. Abstract: The endoplasmic reticulum (ER), mitochondria and lysosomes are physically and/or functionally linked, establishing close contact sites between these organelles. As a consequence, Ca 2+ release events from the ER, the major intracellular Ca 2+ -storage organelle, have an immediate effect on the physiological function of mitochondria and lysosomes. Also, the lysosomes can act as a Ca 2+ source for Ca 2+ release into the cytosol, thereby influencing ER-based Ca 2+ signaling. Given the important role for mitochondria and lysosomes in cell survival, cell death and cell adaptation processes, it has become increasingly clear that Ca 2+ signals from or towards these organelles impact these processes. In this review, we discuss the most recent insights in the emerging role of Ca 2+ signaling in cellular survival by controlling basal mitochondrial bioenergetics and by regulating apoptosis, a mitochondrial process, and autophagy, a lysosomal process, in response to cell damage and cell stress.