2019
DOI: 10.33594/000000192
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Abstract: This article is licensed under the Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License (CC BY-NC-ND). Usage and distribution for commercial purposes as well as any distribution of modified material requires written permission.

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Cited by 9 publications
(5 citation statements)
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References 317 publications
(356 reference statements)
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“…The discovery of ion channels in the IMM was an unexpected outcome of patch-clamp measurements in mitoplasts (mitochondria devoid of the OMM) in the 1980s [ 17 ]. It is now known that abundant K + channels (voltage-gated, Ca 2+ -activated, ATP-dependent, Na + -activated [ 18 ], and two-pore K + channels), as well as Ca 2+ , Na + -, and non-selective cation channels and anion channels participate in ion flows across the IMM [ 19 ]. The roles of the channels may not be limited to canonical ion transport functions, as in some cases direct interactions of particular ion channels, with, for example, components of the electron transport chain (ETC) [ 20 ] or the apoptosis machinery [ 21 ] have been described.…”
Section: Interdependent Ion Fluxes Drive Mitochondrial Functionmentioning
confidence: 99%
See 1 more Smart Citation
“…The discovery of ion channels in the IMM was an unexpected outcome of patch-clamp measurements in mitoplasts (mitochondria devoid of the OMM) in the 1980s [ 17 ]. It is now known that abundant K + channels (voltage-gated, Ca 2+ -activated, ATP-dependent, Na + -activated [ 18 ], and two-pore K + channels), as well as Ca 2+ , Na + -, and non-selective cation channels and anion channels participate in ion flows across the IMM [ 19 ]. The roles of the channels may not be limited to canonical ion transport functions, as in some cases direct interactions of particular ion channels, with, for example, components of the electron transport chain (ETC) [ 20 ] or the apoptosis machinery [ 21 ] have been described.…”
Section: Interdependent Ion Fluxes Drive Mitochondrial Functionmentioning
confidence: 99%
“…K V 1.3 participates in programmed cell death acting downstream of Bax and Bak [ 21 ]. High doses of mitochondria-targeted K V 1.3 inhibitors induce apoptosis, while sublethal concentration increase proliferation [ 19 ], indicating a regulatory role of the channel in the process. Upon specific mitochondrial K V 1.3 inhibition, a transient mitochondrial hyperpolarization followed by cytochrome c release and depolarization precede cell death [ 21 ].…”
Section: Cancer Cell Functions Driven By Changes In Mitochondrial Architecturementioning
confidence: 99%
“…energy conversion and regulation of membrane potential. Mammalian mitochondrial functions represent targets for antibiotics as documented already > 50 years ago [53][54][55][56][57][58][59][60][61][62][63][64][65][66][67][68][69]. Antibiotics interact not only with prokaryotic-and mitochondrial ribosomes but with eukaryotic 80S-ribosomes as well, so that human mitochondria and 80S-ribosomes represent a cancer target for antibiotics, too [70][71][72][73][74].…”
Section: Antibiotics Target Mitochondrial Functions and Inhibit Cancementioning
confidence: 99%
“…Several additional targets for antibiotics in human cells have been identified (Table 2) However, following effect dichotomies have to be considered: antibiotics could be used as adjunctive therapeutics but long-term use may possibly promote resistance development, tumorigenesis, and obesity. Antibiotics were Mitochondrial dysfunction [63][64][65][66][67][68] Aminoglycosides [287] Oxazolidinones (68, 288, 289, S49) Tetracyclines (69, 287, S44 S66) Chloramphenicol (S42, S43) Clinical trials have demonstrated a benefit from treatment of various cancers with aminoglycosides [223] and macrolides (76, S30-S35) Tetracyclines, Tigecycline 28S small mitosomal ribosome [63,295] 28S small mitosomal ribosome [78,79] Mitochondrial dysfunction (63-69, 287, S44, S66) Clinical trials have demonstrated a benefit from treatment of various cancers with tetracyclines (S69-S71) The all-cause mortality was reduced in cancer patients prophylaxed or treated for infections with tigecycline versus patients receiving placebo or no antibacterial treatment [79,405,406]. Combination therapy with piperacillin/ tazobactam increased the survival rate [407] Rifampicin Mitochondrial DNA-dependent RNA polymerase [72] Reduced tumor progression due to suppression of delayed type hypersensitivity; proliferation of spleen lymphocytes (S2, S3)…”
Section: Conclusion and Open Questionsmentioning
confidence: 99%
“…Ca 2+ is fundamental for mitochondrial health, function and metabolism, and sufficient impairments in Ca 2+ homeostasis have detrimental effects on ATP production and cell viability. Thanks to specialized proteins such as MCU, VDAC, NCLX and others, mitochondria are able to modulate their Ca 2+ load in response to pathophysiological conditions, leading either to cell proliferation or cell growth arrest and death [25][26][27][28][29]. Nevertheless, the literature is still conflicting on the nature of Ca 2+ transfer necessary to trigger programmed cell death.…”
Section: Introductionmentioning
confidence: 99%