2011
DOI: 10.1016/j.ceca.2011.04.007
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Mitochondrial permeability transition in Ca2+-dependent apoptosis and necrosis

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Cited by 491 publications
(347 citation statements)
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“…20 As to its cellular function, mitochondrial Ca 2+ has been shown to stimulate ATP production by positive regulation of three key dehydrogenases of the tricarboxylic acid cycle 21 and of the ETC. 22 In parallel, unregulated and sustained organelle Ca 2+ overload can also lead to the opening of the mitochondrial permeability transition pore, 23,24 with consequent dissipation of mitochondrial membrane potential (ΔΨ mt ), release of caspase cofactors and activation of the apoptotic cascade. 5 Despite the significant molecular understanding of all these cellular processes, their role in the pathogenesis of mitochondrial diseases is still poorly understood.…”
mentioning
confidence: 99%
“…20 As to its cellular function, mitochondrial Ca 2+ has been shown to stimulate ATP production by positive regulation of three key dehydrogenases of the tricarboxylic acid cycle 21 and of the ETC. 22 In parallel, unregulated and sustained organelle Ca 2+ overload can also lead to the opening of the mitochondrial permeability transition pore, 23,24 with consequent dissipation of mitochondrial membrane potential (ΔΨ mt ), release of caspase cofactors and activation of the apoptotic cascade. 5 Despite the significant molecular understanding of all these cellular processes, their role in the pathogenesis of mitochondrial diseases is still poorly understood.…”
mentioning
confidence: 99%
“…13 Mitochondrial permeability transition (MPT) is a key event that occurs in most forms of cell demise (apoptotic, necrotic, autophagic or mitotic), determining the life and death of cells. [14][15][16] The opening of MPT pores causes an abrupt increase of inner mitochondrial membrane permeability to solutes with molecular masses of o1500 Da, 14,16,17 leading to mitochondrial swelling, disruption of the mitochondrial outer membranes and mitochondrial dysfunction. 14-16 Keywords: mitochondria; ASIC1a; MPT; oxidative cell death Abbreviations: Aldh7a1, aldehyde dehydrogenase 7 family member a1; AMI, amiloride; ANT, adenine nucleotide translocase; ASIC1a, acid-sensing ion channel 1a; [Ca 2 þ ] em , extramitochondrial Ca 2 þ concentrations; CRC, Ca 2 þ retention capacity; CsA, cyclosporin A; CTB, Cell-Titer Blue; CypD, cyclophilin D; Cyt C, cytochrome c; DNP, dinitrophenol; DC m , mitochondrial membrane potential; GAPDH, glyceraldehyde-3-phosphate dehydrogenase; Gpd2, glycerol-3-phosphate dehydrogenase 2; Hibch, 3-hydroxyisobutyryl-CoA hydrolase; H 2 O 2 , hydrogen peroxide; MCU, mitochondrial Ca 2 þ uniporter; Mito-DsRed, mitochondrion-targeting red fluorescent protein; MPT, mitochondrial permeability transition; mtASIC1a, mitochondrial ASIC1a; MTCO2, cytochrome c oxidase subunit 2; Mterfd2, mitochondria transcription termination factor domain containing 2; PcTX1, psalmotoxin 1; PDI, protein disulfide isomerase; PI, propidium iodide; Pick1, protein interacting with protein kinase C 1; PIN1peptidylprolyl cis/trans isomerase NIMA-interacting 1; ROS, reactive oxygen species; Slc25a25, solute carrier family 25 member 25; TMRM, tetramethylrhodamine methylester; VDAC, voltage-dependent anion channel…”
mentioning
confidence: 99%
“…13 Mitochondrial permeability transition (MPT) is a key event that occurs in most forms of cell demise (apoptotic, necrotic, autophagic or mitotic), determining the life and death of cells. [14][15][16] The opening of MPT pores causes an abrupt increase of inner mitochondrial membrane permeability to solutes with molecular masses of o1500 Da, 14,16,17 leading to mitochondrial swelling, disruption of the mitochondrial outer membranes and mitochondrial dysfunction. [14][15][16] During brain ischemia, the lack of oxygen and glucose causes mitochondrial dysfunction, disrupted intracellular Ca 2 þ homeostasis, increased reactive oxygen species (ROS) production and decreased ATP levels.…”
mentioning
confidence: 99%
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