2021
DOI: 10.3390/cells10061317
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Mitochondrial Ca2+ Signaling in Health, Disease and Therapy

Abstract: The divalent cation calcium (Ca2+) is considered one of the main second messengers inside cells and acts as the most prominent signal in a plethora of biological processes. Its homeostasis is guaranteed by an intricate and complex system of channels, pumps, and exchangers. In this context, by regulating cellular Ca2+ levels, mitochondria control both the uptake and release of Ca2+. Therefore, at the mitochondrial level, Ca2+ plays a dual role, participating in both vital physiological processes (ATP production… Show more

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Cited by 74 publications
(62 citation statements)
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“…One of the first studies proposing a role of mitochondria in age-related dysfunction is dated 1972, when Harman and colleagues [22] hypothesized mitochondria as the main source of ROS. Furthermore, the interplay with the EC coupling system is an important factor to be taken into consideration, as prolonged increases in intracellular Ca 2+ levels caused by dysfunctional EC coupling may cause excessive Ca 2+ uptake by mitochondria, which in turn may lead to mitochondrial dysfunction and possibly to death of cardiomyocytes [7,23]. Marks and colleagues proposed mitochondrial Ca 2+ overload as a key event in HF, as it determines improper ATP production and increased ROS production [24].…”
Section: Introductionmentioning
confidence: 99%
“…One of the first studies proposing a role of mitochondria in age-related dysfunction is dated 1972, when Harman and colleagues [22] hypothesized mitochondria as the main source of ROS. Furthermore, the interplay with the EC coupling system is an important factor to be taken into consideration, as prolonged increases in intracellular Ca 2+ levels caused by dysfunctional EC coupling may cause excessive Ca 2+ uptake by mitochondria, which in turn may lead to mitochondrial dysfunction and possibly to death of cardiomyocytes [7,23]. Marks and colleagues proposed mitochondrial Ca 2+ overload as a key event in HF, as it determines improper ATP production and increased ROS production [24].…”
Section: Introductionmentioning
confidence: 99%
“…The mETC is composed of 5 complexes: NADH-quinone oxidoreductase (Complex I), succinate dehydrogenase (Complex II), coenzyme Q-cytochrome C oxidoreductase (Complex III), cytochrome C oxidase (Complex IV), and ATP synthase (Complex V) [ 52 ]. The Krebs cycle, which is a Ca 2+ -dependent process [ 92 ], generates FADH 2 or NADH that serve as electron donors for four complexes (I-IV) in the mETC, each catalyzing the reduction of O 2 to H 2 O through a single-electron transfer reaction [ 46 ]. Indeed, 1%-2% of the O 2 consumed is estimated to be converted into ROS and not into water [ 69 ].…”
Section: Ros Production and Elimination In Endothelial Cellsmentioning
confidence: 99%
“…(12) Consequently, cytochrome c (Cyt c) is released, thus promoting apoptotic cell death (13). ICS, intracristal space (see [57,58,[60][61][62][63][64][65][66][67][68]). These events are exacerbated by nitric oxide (NO), a key diffusible byproduct of aluminum phthalocyanine chloride photoactivation in irradiated cells [20].…”
Section: Translational Significance Of These Studiesmentioning
confidence: 99%
“…In addition, NO can inhibit the ETC, particularly complex IV, but also complex I, III, and II, by imparting modifications, such as S-nitrosation and nitration to selected residues [70]. Inhibition of complex IV by NO enhances the production of mitochondrial ROS [68]. The combination of NO with superoxide anion can generate peroxinitrite, a potentially harmful radical that drives nitration and oxidation of biomolecules [70].…”
Section: Translational Significance Of These Studiesmentioning
confidence: 99%