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Journal articles on the topic 'Unipore calcique mitochondrial'

Author: Grafiati

Published: 24 May 2025

Last updated: 29 May 2025

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1

Wang, Guang Jian, and Stanley A. Thayer. "NMDA-Induced Calcium Loads Recycle Across the Mitochondrial Inner Membrane of Hippocampal Neurons in Culture." Journal of Neurophysiology 87, no. 2 (2002): 740–49. http://dx.doi.org/10.1152/jn.00345.2001.

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Mitochondria sequester N-methyl-d-aspartate (NMDA)-induced Ca2+ loads and regulate the shape of intracellular Ca2+ concentration ([Ca2+]i) responses in neurons. When isolated mitochondria are exposed to high [Ca2+],Ca2+ enters the matrix via the uniporter and returns to the cytosol by Na+/Ca2+ exchange. Released Ca2+ may re-enter the mitochondrion recycling across the inner membrane dissipating respiratory energy. Ca2+ recycling, the continuous uptake and release of Ca2+ by mitochondria, has not been described in intact neurons. Here we used single-cell microfluorimetry to measure [Ca2+]i and

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2

Dubinin, Mikhail V., Eugeny Yu Talanov, Kirill S. Tenkov, Vlada S. Starinets, Natalia V. Belosludtseva, and Konstantin N. Belosludtsev. "The Effect of Deflazacort Treatment on the Functioning of Skeletal Muscle Mitochondria in Duchenne Muscular Dystrophy." International Journal of Molecular Sciences 21, no. 22 (2020): 8763. http://dx.doi.org/10.3390/ijms21228763.

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Duchenne muscular dystrophy (DMD) is a severe hereditary disease caused by a lack of dystrophin, a protein essential for myocyte integrity. Mitochondrial dysfunction is reportedly responsible for DMD. This study examines the effect of glucocorticoid deflazacort on the functioning of the skeletal-muscle mitochondria of dystrophin-deficient mdx mice and WT animals. Deflazacort administration was found to improve mitochondrial respiration of mdx mice due to an increase in the level of ETC complexes (complexes III and IV and ATP synthase), which may contribute to the normalization of ATP levels in

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Rimessi, Alessandro, Chiara Pozzato, Lorenzo Carparelli, et al. "Pharmacological modulation of mitochondrial calcium uniporter controls lung inflammation in cystic fibrosis." Science Advances 6, no. 19 (2020): eaax9093. http://dx.doi.org/10.1126/sciadv.aax9093.

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Mitochondria physically associate with the endoplasmic reticulum to coordinate interorganelle calcium transfer and regulate fundamental cellular processes, including inflammation. Deregulated endoplasmic reticulum–mitochondria cross-talk can occur in cystic fibrosis, contributing to hyperinflammation and disease progression. We demonstrate that Pseudomonas aeruginosa infection increases endoplasmic reticulum–mitochondria associations in cystic fibrosis bronchial cells by stabilizing VAPB-PTPIP51 (vesicle-associated membrane protein–associated protein B–protein tyrosine phosphatase interacting

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4

Naon, Deborah, Marta Zaninello, Marta Giacomello, et al. "Critical reappraisal confirms that Mitofusin 2 is an endoplasmic reticulum–mitochondria tether." Proceedings of the National Academy of Sciences 113, no. 40 (2016): 11249–54. http://dx.doi.org/10.1073/pnas.1606786113.

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The discovery of the multiple roles of mitochondria–endoplasmic reticulum (ER) juxtaposition in cell biology often relied upon the exploitation of Mitofusin (Mfn) 2 as an ER–mitochondria tether. However, this established Mfn2 function was recently questioned, calling for a critical re-evaluation of Mfn2’s role in ER–mitochondria cross-talk. Electron microscopy and fluorescence-based probes of organelle proximity confirmed that ER–mitochondria juxtaposition was reduced by constitutive or acute Mfn2 deletion. Functionally, mitochondrial uptake of Ca2+ released from the ER was reduced following a

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5

Tedesco, Scattolini, Albiero, et al. "Mitochondrial Calcium Uptake Is Instrumental to Alternative Macrophage Polarization and Phagocytic Activity." International Journal of Molecular Sciences 20, no. 19 (2019): 4966. http://dx.doi.org/10.3390/ijms20194966.

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Macrophages are highly plastic and dynamic cells that exert much of their function through phagocytosis. Phagocytosis depends on a coordinated, finely tuned, and compartmentalized regulation of calcium concentrations. We examined the role of mitochondrial calcium uptake and mitochondrial calcium uniporter (MCU) in macrophage polarization and function. In primary cultures of human monocyte-derived macrophages, calcium uptake in mitochondria was instrumental for alternative (M2) macrophage polarization. Mitochondrial calcium uniporter inhibition with KB-R7943 or MCU knockdown, which prevented mi

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6

Zhang, Linlin, Jingyi Qi, Xu Zhang, et al. "The Regulatory Roles of Mitochondrial Calcium and the Mitochondrial Calcium Uniporter in Tumor Cells." International Journal of Molecular Sciences 23, no. 12 (2022): 6667. http://dx.doi.org/10.3390/ijms23126667.

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Mitochondria, as the main site of cellular energy metabolism and the generation of oxygen free radicals, are the key switch for mitochondria-mediated endogenous apoptosis. Ca2+ is not only an important messenger for cell proliferation, but it is also an indispensable signal for cell death. Ca2+ participates in and plays a crucial role in the energy metabolism, physiology, and pathology of mitochondria. Mitochondria control the uptake and release of Ca2+ through channels/transporters, such as the mitochondrial calcium uniporter (MCU), and influence the concentration of Ca2+ in both mitochondria

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7

MONTERO, Mayte, Carmen D. LOBATÓN, Esther HERNÁNDEZ-SANMIGUEL, et al. "Direct activation of the mitochondrial calcium uniporter by natural plant flavonoids." Biochemical Journal 384, no. 1 (2004): 19–24. http://dx.doi.org/10.1042/bj20040990.

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During cell activation, mitochondria play an important role in Ca2+ homoeostasis due to the presence of a fast and specific Ca2+ channel in its inner membrane, the mitochondrial Ca2+ uniporter. This channel allows mitochondria to buffer local cytosolic [Ca2+] changes and controls the intramitochondrial Ca2+ levels, thus modulating a variety of phenomena from respiratory rate to apoptosis. We have described recently that SB202190, an inhibitor of p38 MAPK (mitogen-activated protein kinase), strongly activated the uniporter. We show in the present study that a series of natural plant flavonoids,

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Satrústegui, Jorgina, Beatriz Pardo, and Araceli del Arco. "Mitochondrial Transporters as Novel Targets for Intracellular Calcium Signaling." Physiological Reviews 87, no. 1 (2007): 29–67. http://dx.doi.org/10.1152/physrev.00005.2006.

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Ca2+signaling in mitochondria is important to tune mitochondrial function to a variety of extracellular stimuli. The main mechanism is Ca2+entry in mitochondria via the Ca2+uniporter followed by Ca2+activation of three dehydrogenases in the mitochondrial matrix. This results in increases in mitochondrial NADH/NAD ratios and ATP levels and increased substrate uptake by mitochondria. We review evidence gathered more than 20 years ago and recent work indicating that substrate uptake, mitochondrial NADH/NAD ratios, and ATP levels may be also activated in response to cytosolic Ca2+signals via a mec

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9

Tsai, Chen-Wei, Yujiao Wu, Ping-Chieh Pao, et al. "Proteolytic control of the mitochondrial calcium uniporter complex." Proceedings of the National Academy of Sciences 114, no. 17 (2017): 4388–93. http://dx.doi.org/10.1073/pnas.1702938114.

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The mitochondrial calcium uniporter is a Ca2+-activated Ca2+ channel complex mediating mitochondrial Ca2+ uptake, a process crucial for Ca2+ signaling, bioenergetics, and cell death. The uniporter is composed of the pore-forming MCU protein, the gatekeeping MICU1 and MICU2 subunits, and EMRE, a single-pass membrane protein that links MCU and MICU1 together. As a bridging subunit required for channel function, EMRE could paradoxically inhibit uniporter complex formation if expressed in excess. Here, we show that mitochondrial mAAA proteases AFG3L2 and SPG7 rapidly degrade unassembled EMRE using

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10

Zavodnik, I. B. "Mitochondria, calcium homeostasis and calcium signaling." Biomeditsinskaya Khimiya 62, no. 3 (2016): 311–17. http://dx.doi.org/10.18097/pbmc20166203311.

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Са2+ is a very important and versatile intracellular signal which controls numerous biochemical and physiological (pathophysiological) processes in the cell. Good evidence exists that mitochondria are sensors, decoders and regulators of calcium signaling. Precise regulation of calcium signaling in the cell involves numerous molecular targets, which induce and decode changes of Са2+ concentrations in the cell (pumps, channels, Са2+-binding proteins, Са2+-dependent enzymes, localized in the cytoplasm and organelles). Mitochondrial Са2+ uniporter accumulates excess of Са2+ in mitochondria, while

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11

Peng, Wesley, Yvette C. Wong, and Dimitri Krainc. "Mitochondria-lysosome contacts regulate mitochondrial Ca2+dynamics via lysosomal TRPML1." Proceedings of the National Academy of Sciences 117, no. 32 (2020): 19266–75. http://dx.doi.org/10.1073/pnas.2003236117.

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Mitochondria and lysosomes are critical for cellular homeostasis, and dysfunction of both organelles has been implicated in numerous diseases. Recently, interorganelle contacts between mitochondria and lysosomes were identified and found to regulate mitochondrial dynamics. However, whether mitochondria–lysosome contacts serve additional functions by facilitating the direct transfer of metabolites or ions between the two organelles has not been elucidated. Here, using high spatial and temporal resolution live-cell microscopy, we identified a role for mitochondria–lysosome contacts in regulating

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12

Gavin, C. E., K. K. Gunter, and T. E. Gunter. "Manganese and calcium efflux kinetics in brain mitochondria. Relevance to manganese toxicity." Biochemical Journal 266, no. 2 (1990): 329–34. http://dx.doi.org/10.1042/bj2660329.

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Manganese shares the uniport mechanism of mitochondrial calcium influx, accumulates in mitochondria and is cleared only very slowly from brain. Using dual-label isotope techniques, we have investigated both Mn2+ and Ca2+ mitochondrial efflux kinetics. We report that (1) there is no significant Na(+)-dependent Mn2+ efflux from brain mitochondria; (2) Mn2+ inhibits both Na(+)-dependent and Na(+)-independent Ca2+ efflux in brain, in a mode that appears to be primarily competitive and with apparent Ki values of 5.1 and 7.9 nmol/mg respectively; and (3) Ca2+ does not appear to inhibit Mn2+ efflux f

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13

Duchen, Michael R., Anne Leyssens, and Martin Crompton. "Transient Mitochondrial Depolarizations Reflect Focal Sarcoplasmic Reticular Calcium Release in Single Rat Cardiomyocytes." Journal of Cell Biology 142, no. 4 (1998): 975–88. http://dx.doi.org/10.1083/jcb.142.4.975.

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Digital imaging of mitochondrial potential in single rat cardiomyocytes revealed transient depolarizations of mitochondria discretely localized within the cell, a phenomenon that we shall call “flicker.” These events were usually highly localized and could be restricted to single mitochondria, but they could also be more widely distributed within the cell. Contractile waves, either spontaneous or in response to depolarization with 50 mM K+, were associated with propagating waves of mitochondrial depolarization, suggesting that propagating calcium waves are associated with mitochondrial calcium

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14

Lee, Andy K., and Amy Tse. "Dominant Role of Mitochondria in Calcium Homeostasis of Single Rat Pituitary Corticotropes." Endocrinology 146, no. 11 (2005): 4985–93. http://dx.doi.org/10.1210/en.2005-0358.

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The rise in cytosolic free Ca2+ concentration ([Ca2+]i) is the major trigger for secretion of ACTH from pituitary corticotropes. To better understand the shaping of the Ca2+ signal in corticotropes, we investigated the mechanisms regulating the depolarization-triggered Ca2+ signal using patch-clamp techniques and indo-1 fluorometry. The rate of cytosolic Ca2+ clearance was unaffected by inhibitors of Na+/Ca2+ exchanger or plasma membrane Ca2+-ATPase (PMCA), slightly slowed by sarco-endoplasmic reticulum Ca2+-ATPase (SERCA) inhibitor, but dramatically slowed by mitochondrial uncouplers or inhib

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15

Zavodnik, I. B., T. A. Kovalenia, A. G. Veiko, et al. "Structural and functional changes in rat liver mitochondria under calcium ion loading in the absence and presence of flavonoids." Biomeditsinskaya Khimiya 68, no. 4 (2022): 237–49. http://dx.doi.org/10.18097/pbmc20226804237.

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The aim of the present work was to elucidate the mechanisms of calcium ion-induced impairments of the ultrastructure and functional activity of isolated rat liver mitochondria in the absence and presence of a number of flavonoids in vitro. In the presence of exogenous Ca2+ (20-60 μM), mitochondrial heterogeneity in size and electron density markedly increased: most organelles demonstrated a swollen electron-light matrix, bigger size, elongated cristae and a reduced their number, a damaged native structure of the inner membrane up to its detachment, and some mitochondria showed a more electron-

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16

Zhang, Ruobing. "Mitochondrial proteins that connected with calcium: do their pathways changes in PAH?" BIO Web of Conferences 55 (2022): 01018. http://dx.doi.org/10.1051/bioconf/20225501018.

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Calcium can be regulated by mitochondria and also plays a significant role in mitochondrial pathways. Recent study showed mitochondrial protein changes in the right ventricle in pulmonary arterial hypertension, which affects calcium network at the same time. The specific objective of this study is to assess the pathway of calcium transport by permeable pore in mitochondria and investigate the regulation of mitochondrial proteins in order to find the connection between mitochondrial proteins and right ventricular dysfunction in PAH (pulmonary arterial hypertension). This literature-based review

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17

Sanganahalli, Basavaraju G., Peter Herman, Fahmeed Hyder, and Sridhar S. Kannurpatti. "Mitochondrial Calcium Uptake Capacity Modulates Neocortical Excitability." Journal of Cerebral Blood Flow & Metabolism 33, no. 7 (2013): 1115–26. http://dx.doi.org/10.1038/jcbfm.2013.61.

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Local calcium (Ca2 +) changes regulate central nervous system metabolism and communication integrated by subcellular processes including mitochondrial Ca2 + uptake. Mitochondria take up Ca2 + through the calcium uniporter (mCU) aided by cytoplasmic microdomains of high Ca2 +. Known only in vitro, the in vivo impact of mCU activity may reveal Ca2 + -mediated roles of mitochondria in brain signaling and metabolism. From in vitro studies of mitochondrial Ca2 + sequestration and cycling in various cell types of the central nervous system, we evaluated ranges of spontaneous and activity-induced Ca2

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18

Kannurpatti, Sridhar S. "Mitochondrial calcium homeostasis: Implications for neurovascular and neurometabolic coupling." Journal of Cerebral Blood Flow & Metabolism 37, no. 2 (2016): 381–95. http://dx.doi.org/10.1177/0271678x16680637.

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Mitochondrial function is critical to maintain high rates of oxidative metabolism supporting energy demands of both spontaneous and evoked neuronal activity in the brain. Mitochondria not only regulate energy metabolism, but also influence neuronal signaling. Regulation of “energy metabolism” and “neuronal signaling” (i.e. neurometabolic coupling), which are coupled rather than independent can be understood through mitochondria’s integrative functions of calcium ion (Ca2+) uptake and cycling. While mitochondrial Ca2+ do not affect hemodynamics directly, neuronal activity changes are mechanisti

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Zhang, Xinyi, Shuhu Liu, Yanshan Su, Ling Zhang, Ting Guo, and Xuemin Wang. "Sirtuin-1 Regulates Mitochondrial Calcium Uptake Through Mitochondrial Calcium Uptake 1 (MICU1)." Life 15, no. 2 (2025): 174. https://doi.org/10.3390/life15020174.

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Mitochondria play a central role in cell biological processes, functioning not only as producers of ATP but also as regulators of Ca2+ signaling. Mitochondrial calcium uptake occurs primarily through the mitochondrial calcium uniporter channel (mtCU), with the mitochondrial calcium uptake subunits 1, 2, and 3 (MICU1, MICU2, and MICU3) serving as the main regulatory components. Dysregulated mitochondrial calcium uptake is a hallmark of cellular degeneration. Sirtuin 1 (SIRT1), a key regulator of cellular metabolism, plays a critical role in aging and various neurodegenerative conditions. By blo

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20

D’Angelo, Donato, and Rosario Rizzuto. "The Mitochondrial Calcium Uniporter (MCU): Molecular Identity and Role in Human Diseases." Biomolecules 13, no. 9 (2023): 1304. http://dx.doi.org/10.3390/biom13091304.

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Calcium (Ca2+) ions act as a second messenger, regulating several cell functions. Mitochondria are critical organelles for the regulation of intracellular Ca2+. Mitochondrial calcium (mtCa2+) uptake is ensured by the presence in the inner mitochondrial membrane (IMM) of the mitochondrial calcium uniporter (MCU) complex, a macromolecular structure composed of pore-forming and regulatory subunits. MtCa2+ uptake plays a crucial role in the regulation of oxidative metabolism and cell death. A lot of evidence demonstrates that the dysregulation of mtCa2+ homeostasis can have serious pathological ou

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21

Granatiero, Veronica, Marco Pacifici, Anna Raffaello, Diego De Stefani, and Rosario Rizzuto. "Overexpression of Mitochondrial Calcium Uniporter Causes Neuronal Death." Oxidative Medicine and Cellular Longevity 2019 (October 16, 2019): 1–15. http://dx.doi.org/10.1155/2019/1681254.

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Neurodegenerative diseases are a large and heterogeneous group of disorders characterized by selective and progressive death of specific neuronal subtypes. In most of the cases, the pathophysiology is still poorly understood, although a number of hypotheses have been proposed. Among these, dysregulation of Ca2+ homeostasis and mitochondrial dysfunction represent two broadly recognized early events associated with neurodegeneration. However, a direct link between these two hypotheses can be drawn. Mitochondria actively participate to global Ca2+ signaling, and increases of [Ca2+] inside organel

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Wen, Haitao, Tianliang Li, Xinghui Li, Yu Lei, and Douglas R. Green. "Mitochondrial Calcium Signaling Facilitates Bacterial Survival by Restraining LC3-associated Phagocytosis." Journal of Immunology 204, no. 1_Supplement (2020): 227.1. http://dx.doi.org/10.4049/jimmunol.204.supp.227.1.

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Abstract Mitochondria in eukaryotic cells are believed to have originated from proteobacteria through endosymbiosis 2.5 billion years ago. Accumulating evidence suggests essential roles of mitochondria in host defense response against invading pathogens. Whether intracellular bacteria can hijack mitochondria to promote their survival remains elusive. Here, we demonstrate a previously unappreciated pro-survival strategy employed by intracellular bacteria Listeria monocytogenesthat involves the suppression of LC3-associated phagocytosis (LAP) by mitochondrial Ca2+ signaling. Invasion of macropha

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Pallafacchina, Giorgia, Sofia Zanin, and Rosario Rizzuto. "From the Identification to the Dissection of the Physiological Role of the Mitochondrial Calcium Uniporter: An Ongoing Story." Biomolecules 11, no. 6 (2021): 786. http://dx.doi.org/10.3390/biom11060786.

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The notion of mitochondria being involved in the decoding and shaping of intracellular Ca2+ signals has been circulating since the end of the 19th century. Despite that, the molecular identity of the channel that mediates Ca2+ ion transport into mitochondria remained elusive for several years. Only in the last decade, the genes and pathways responsible for the mitochondrial uptake of Ca2+ began to be cloned and characterized. The gene coding for the pore-forming unit of the mitochondrial channel was discovered exactly 10 years ago, and its product was called mitochondrial Ca2+ uniporter or MCU

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Chakrabarti, Rajarshi, Wei-Ke Ji, Radu V. Stan, Jaime de Juan Sanz, Timothy A. Ryan, and Henry N. Higgs. "INF2-mediated actin polymerization at the ER stimulates mitochondrial calcium uptake, inner membrane constriction, and division." Journal of Cell Biology 217, no. 1 (2017): 251–68. http://dx.doi.org/10.1083/jcb.201709111.

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Mitochondrial division requires division of both the inner and outer mitochondrial membranes (IMM and OMM, respectively). Interaction with endoplasmic reticulum (ER) promotes OMM division by recruitment of the dynamin Drp1, but effects on IMM division are not well characterized. We previously showed that actin polymerization through ER-bound inverted formin 2 (INF2) stimulates Drp1 recruitment in mammalian cells. Here, we show that INF2-mediated actin polymerization stimulates a second mitochondrial response independent of Drp1: a rise in mitochondrial matrix calcium through the mitochondrial

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Ajanel Gomez, Abigail, Frederik Denorme, Irina Portier, et al. "Platelet Mitochondria Calcium Uniporter Regulates ITAM-Dependent Platelet Activation and Signaling." Blood 142, Supplement 1 (2023): 1187. http://dx.doi.org/10.1182/blood-2023-189538.

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Introduction: The ability of platelets to multitask is critical to arrest bleeding after injury and for the development of arterial thrombosis, which underlies myocardial infarction and stroke. Platelet activation relies heavily on changes in cytoplasmic calcium flux. However, little is known on the role mitochondrial calcium flux directly plays in platelet activation. In other cells, release of calcium from intracellular stores results in calcium entry into channels located in the outer mitochondrial membrane. Once calcium enters the intermembrane space, entry into the mitochondrial matrix is

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Brisac, Cynthia, François Téoulé, Arnaud Autret, et al. "Calcium Flux between the Endoplasmic Reticulum and Mitochondrion Contributes to Poliovirus-Induced Apoptosis." Journal of Virology 84, no. 23 (2010): 12226–35. http://dx.doi.org/10.1128/jvi.00994-10.

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ABSTRACT We show that poliovirus (PV) infection induces an increase in cytosolic calcium (Ca2+) concentration in neuroblastoma IMR5 cells, at least partly through Ca2+ release from the endoplasmic reticulum lumen via the inositol 1,4,5-triphosphate receptor (IP3R) and ryanodine receptor (RyR) channels. This leads to Ca2+ accumulation in mitochondria through the mitochondrial Ca2+ uniporter and the voltage-dependent anion channel (VDAC). This increase in mitochondrial Ca2+ concentration in PV-infected cells leads to mitochondrial dysfunction and apoptosis.

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27

Sun, Zhe, Zicheng Ma, Wandi Cao, et al. "Calcium-mediated mitochondrial fission and mitophagy drive glycolysis to facilitate arterivirus proliferation." PLOS Pathogens 21, no. 1 (2025): e1012872. https://doi.org/10.1371/journal.ppat.1012872.

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Mitochondria, recognized as the “powerhouse” of cells, play a vital role in generating cellular energy through dynamic processes such as fission and fusion. Viruses have evolved mechanisms to hijack mitochondrial function for their survival and proliferation. Here, we report that infection with the swine arterivirus porcine reproductive and respiratory syndrome virus (PRRSV), manipulates mitochondria calcium ions (Ca2+) to induce mitochondrial fission and mitophagy, thereby reprogramming cellular energy metabolism to facilitate its own replication. Mechanistically, PRRSV-induced mitochondrial

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Rolo, Anabela P., Paulo J. Oliveira, António J. M. Moreno, and Carlos M. Palmeira. "Chenodeoxycholate Is a Potent Inducer of the Permeability Transition Pore in Rat Liver Mitochondria." Bioscience Reports 21, no. 1 (2001): 73–80. http://dx.doi.org/10.1023/a:1010438202519.

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Several reports support the concept that bile acids may be cytotoxic during cholestatic disease process by causing mitochondrial dysfunction. Here we report additional data and findings aimed at a better understanding of the involvement of the permeability transition pore (PTP) opening in bile acids toxicity. The mitochondrial PTP is implicated as a mediator of cell injury and death in many situations. In the presence of calcium and phosphate, chenodeoxycholic acid (CDCA) induced a permeability transition in freshly isolated rat liver mitochondria, characterized by membrane depolarization, rel

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Venugopal, Anila, Mahalaxmi Iyer, Venkatesh Balasubramanian, and Balachandar Vellingiri. "Mitochondrial calcium uniporter as a potential therapeutic strategy for Alzheimer’s disease." Acta Neuropsychiatrica 32, no. 2 (2019): 65–71. http://dx.doi.org/10.1017/neu.2019.39.

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AbstractAlzheimer’s disease (AD), a neurodegenerative disorder, is the leading cause of dementia in the world whose aetiology is still unclear. AD was always related to ageing though there have been instances where people at an early age also succumb to this disease. With medical advancements, the mortality rate has significantly reduced which also makes people more prone to AD. AD is rare, yet the prominent disease has been widely studied with several hypotheses trying to understand the workings of its onset. The most recent and popular hypothesis in AD is the involvement of mitochondrial dys

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Weinberg, J. M., and H. D. Humes. "Calcium transport and inner mitochondrial membrane damage in renal cortical mitochondria." American Journal of Physiology-Renal Physiology 248, no. 6 (1985): F876—F889. http://dx.doi.org/10.1152/ajprenal.1985.248.6.f876.

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Ca2+ uptake and efflux processes, as they are manifested during procedures used for isolation of renal cortical mitochondria, were characterized in order to provide a better basis for making inferences from isolated mitochondria about the in vivo state of mitochondrial Ca2+ homeostasis in both normal and injured tissues and to better define the mechanisms by which Ca2+ mediates injury to renal cortical mitochondria. Mitochondrial Ca2+ uptake predictably occurred when the capacity of the Ca2+ chelator added to the isolating medium to maintain free Ca2+ in the submicromolar range was exhausted u

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Lee, Sandra H., Hannah E. Duron, and Dipayan Chaudhuri. "Beyond the TCA cycle: new insights into mitochondrial calcium regulation of oxidative phosphorylation." Biochemical Society Transactions 51, no. 4 (2023): 1661–73. http://dx.doi.org/10.1042/bst20230012.

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While mitochondria oxidative phosphorylation is broadly regulated, the impact of mitochondrial Ca2+ on substrate flux under both physiological and pathological conditions is increasingly being recognized. Under physiologic conditions, mitochondrial Ca2+ enters through the mitochondrial Ca2+ uniporter and boosts ATP production. However, maintaining Ca2+ homeostasis is crucial as too little Ca2+ inhibits adaptation to stress and Ca2+ overload can trigger cell death. In this review, we discuss new insights obtained over the past several years expanding the relationship between mitochondrial Ca2+

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Zhang, Dejiu, Fei Wang, Peifeng Li, and Yanyan Gao. "Mitochondrial Ca2+ Homeostasis: Emerging Roles and Clinical Significance in Cardiac Remodeling." International Journal of Molecular Sciences 23, no. 6 (2022): 3025. http://dx.doi.org/10.3390/ijms23063025.

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Mitochondria are the sites of oxidative metabolism in eukaryotes where the metabolites of sugars, fats, and amino acids are oxidized to harvest energy. Notably, mitochondria store Ca2+ and work in synergy with organelles such as the endoplasmic reticulum and extracellular matrix to control the dynamic balance of Ca2+ concentration in cells. Mitochondria are the vital organelles in heart tissue. Mitochondrial Ca2+ homeostasis is particularly important for maintaining the physiological and pathological mechanisms of the heart. Mitochondrial Ca2+ homeostasis plays a key role in the regulation of

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Gunter, T. E., and D. R. Pfeiffer. "Mechanisms by which mitochondria transport calcium." American Journal of Physiology-Cell Physiology 258, no. 5 (1990): C755—C786. http://dx.doi.org/10.1152/ajpcell.1990.258.5.c755.

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It has been firmly established that the rapid uptake of Ca2+ by mitochondria from a wide range of sources is mediated by a uniporter which permits transport of the ion down its electrochemical gradient. Several mechanisms of Ca2+ efflux from mitochondria have also been extensively discussed in the literature. Energized mitochondria must expend a significant amount of energy to transport Ca2+ against its electrochemical gradient from the matrix space to the external space. Two separate mechanisms have been found to mediate this outward transport: a Ca2+/nNa+ exchanger and a Na(+)-independent ef

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Sander, Paulina, Thomas Gudermann, and Johann Schredelseker. "A Calcium Guard in the Outer Membrane: Is VDAC a Regulated Gatekeeper of Mitochondrial Calcium Uptake?" International Journal of Molecular Sciences 22, no. 2 (2021): 946. http://dx.doi.org/10.3390/ijms22020946.

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Already in the early 1960s, researchers noted the potential of mitochondria to take up large amounts of Ca2+. However, the physiological role and the molecular identity of the mitochondrial Ca2+ uptake mechanisms remained elusive for a long time. The identification of the individual components of the mitochondrial calcium uniporter complex (MCUC) in the inner mitochondrial membrane in 2011 started a new era of research on mitochondrial Ca2+ uptake. Today, many studies investigate mitochondrial Ca2+ uptake with a strong focus on function, regulation, and localization of the MCUC. However, on it

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Yun, Bogeon, HeeJung Lee, Moumita Ghosh, et al. "Serine Hydrolase Inhibitors Block Necrotic Cell Death by Preventing Calcium Overload of the Mitochondria and Permeability Transition Pore Formation." Journal of Biological Chemistry 289, no. 3 (2013): 1491–504. http://dx.doi.org/10.1074/jbc.m113.497651.

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Perturbation of calcium signaling that occurs during cell injury and disease, promotes cell death. In mouse lung fibroblasts A23187 triggered mitochondrial permeability transition pore (MPTP) formation, lactate dehydrogenase (LDH) release, and necrotic cell death that were blocked by cyclosporin A (CsA) and EGTA. LDH release temporally correlated with arachidonic acid release but did not involve cytosolic phospholipase A2α (cPLA2α) or calcium-independent PLA2. Surprisingly, release of arachidonic acid and LDH from cPLA2α-deficient fibroblasts was inhibited by the cPLA2α inhibitor pyrrophenone,

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Vlessis, A. A., and L. Mela-Riker. "Potential role of mitochondrial calcium metabolism during reperfusion injury." American Journal of Physiology-Cell Physiology 256, no. 6 (1989): C1196—C1206. http://dx.doi.org/10.1152/ajpcell.1989.256.6.c1196.

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Ischemia-reperfusion injury has been associated with intracellular H2O2 and superoxide radical production from accumulated hypoxanthine (HX) and xanthine oxidase (XO). The effect of H2O2 and superoxide radical on mitochondrial Ca2+ efflux was characterized in isolated renal mitochondria using a HX-XO system. Mitochondria were suspended in buffered medium containing 200 microM HX. Extramitochondrial Ca2+ was monitored kinetically at 660-685 nm using the Ca2+ indicator arsenazo III. After preloading mitochondria with 18-25 nmol Ca2+/mg protein, addition of XO to the medium caused a rapid oxidati

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Weissenrieder, Jillian S., Jason Pitarresi, Natalie Weinmann, et al. "Abstract C113: The mitochondrial calcium uniporter supports epithelial to mesenchymal transition of pancreatic ductal adenocarcinoma." Cancer Research 84, no. 2_Supplement (2024): C113. http://dx.doi.org/10.1158/1538-7445.panca2023-c113.

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Abstract In spite of many new developments in cancer treatments and targeted therapies over the past few decades, outcomes for pancreatic ductal adenocarcinoma (PDAC) patients continue to be poor. Calcium signaling and mitochondrial function are known to contribute to cancer outcomes in many paradigms, yet much remains unknown in the context of PDAC. The mitochondrial Ca2+ uniporter, MCU, is the main route by which mitochondria can take up Ca2+ into the mitochondrial matrix, where it drives metabolic activity in the tricarboxylic acid cycle and promotes ATP synthesis by the electron transport

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Apicco, Daniel J., Evgeny Shlevkov, Catherine L. Nezich та ін. "The Parkinson’s disease-associated gene ITPKB protects against α-synuclein aggregation by regulating ER-to-mitochondria calcium release". Proceedings of the National Academy of Sciences 118, № 1 (2020): e2006476118. http://dx.doi.org/10.1073/pnas.2006476118.

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Inositol-1,4,5-triphosphate (IP3) kinase B (ITPKB) is a ubiquitously expressed lipid kinase that inactivates IP3, a secondary messenger that stimulates calcium release from the endoplasmic reticulum (ER). Genome-wide association studies have identified common variants in the ITPKB gene locus associated with reduced risk of sporadic Parkinson’s disease (PD). Here, we investigate whether ITPKB activity or expression level impacts PD phenotypes in cellular and animal models. In primary neurons, knockdown or pharmacological inhibition of ITPKB increased levels of phosphorylated, insoluble α-synucl

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de la Fuente, Sergio, Rosalba I. Fonteriz, Pedro J. de la Cruz, Mayte Montero, and Javier Alvarez. "Mitochondrial free [Ca2+] dynamics measured with a novel low-Ca2+ affinity aequorin probe." Biochemical Journal 445, no. 3 (2012): 371–76. http://dx.doi.org/10.1042/bj20120423.

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Mitochondria have a very large capacity to accumulate Ca2+ during cell stimulation driven by the mitochondrial membrane potential. Under these conditions, [Ca2+]M (mitochondrial [Ca2+]) may well reach millimolar levels in a few seconds. Measuring the dynamics of [Ca2+]M during prolonged stimulation has been previously precluded by the high Ca2+ affinity of the probes available. We have now developed a mitochondrially targeted double-mutated form of the photoprotein aequorin which is able to measure [Ca2+] in the millimolar range for long periods of time without problems derived from aequorin c

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Motloch, Lukas Jaroslaw, Robert Larbig, Tina Gebing, et al. "Ucp2 Modulates Mitochondrial Calcium Uniporter." Biophysical Journal 106, no. 2 (2014): 593a. http://dx.doi.org/10.1016/j.bpj.2013.11.3282.

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Stoll, Shaunrick, Jing Xi, Ben Ma, et al. "The Valosin-Containing Protein Protects the Heart Against Pathological Ca2+ Overload by Modulating Ca2+ Uptake Proteins." Toxicological Sciences 171, no. 2 (2019): 473–84. http://dx.doi.org/10.1093/toxsci/kfz164.

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Abstract Stress-induced mitochondrial calcium (Ca2+) overload is a key cellular toxic effectors and a trigger of cardiomyocyte death during cardiac ischemic injury through the opening of mitochondrial permeability transition pore (mPTP). We previously found that the valosin-containing protein (VCP), an ATPase-associated protein, protects cardiomyocytes against stress-induced death and also inhibits mPTP opening in vitro. However, the underlying molecular mechanisms are not fully understood. Here, we tested our hypothesis that VCP acts as a novel regulator of mitochondrial Ca2+ uptake proteins

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Dedkova, Elena N., Xiang Ji, Stephen L. Lipsius, and Lothar A. Blatter. "Mitochondrial calcium uptake stimulates nitric oxide production in mitochondria of bovine vascular endothelial cells." American Journal of Physiology-Cell Physiology 286, no. 2 (2004): C406—C415. http://dx.doi.org/10.1152/ajpcell.00155.2003.

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Although nitric oxide (NO) is a known modulator of cell respiration in vascular endothelium, the presence of a mitochondria-specific nitric oxide synthase (mtNOS) in these cells is still a controversial issue. We have used laser scanning confocal microscopy in combination with the NO-sensitive fluorescent dye DAF-2 to monitor changes in NO production by mitochondria of calf vascular endothelial (CPAE) cells. Cells were loaded with the membrane-permeant NO-sensitive dye 4,5-diaminofluorescein (DAF-2) diacetate and subsequently permeabilized with digitonin to remove cytosolic DAF-2 to allow meas

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Tanzarella, Paola, Anna Ferretta, Simona Barile, et al. "Increased Levels of cAMP by the Calcium-Dependent Activation of Soluble Adenylyl Cyclase in Parkin-Mutant Fibroblasts." Cells 8, no. 3 (2019): 250. http://dx.doi.org/10.3390/cells8030250.

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Almost half of autosomal recessive early-onset parkinsonism has been associated with mutations in PARK2, coding for parkin, which plays an important role in mitochondria function and calcium homeostasis. Cyclic adenosine monophosphate (cAMP) is a major second messenger regulating mitochondrial metabolism, and it is strictly interlocked with calcium homeostasis. Parkin-mutant (Pt) fibroblasts, exhibiting defective mitochondrial respiratory/OxPhos activity, showed a significant higher value of basal intracellular level of cAMP, as compared with normal fibroblasts (CTRL). Specific pharmacological

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Dong, Hong, Bao Zhao, and Haitao Wen. "Mitochondrial calcium uniporter positively regulates phagocytosis-dependent activation of NLRP3 inflammasome." Journal of Immunology 206, no. 1_Supplement (2021): 15.01. http://dx.doi.org/10.4049/jimmunol.206.supp.15.01.

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Abstract Mitochondria have been shown to play an essential role in the innate immune function and inflammatory response. Mitochondrial Ca2+ signaling, which is controlled by mitochondrial Ca2+ uniporter (MCU), is a fundamental mechanism regulating mitochondrial metabolism. Accumulative evidence suggests MCU-dependent mitochondrial Ca2+ signaling may bridge the metabolic reprogramming and regulation of immune cell function. However, the mechanism by which MCU regulates inflammation and its related disease remains elusive. Here we report a critical role of MCU in promoting phagocytosis-dependent

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Pandey, Vikas, Lai-Hua Xie, Zhilin Qu, and Zhen Song. "Mitochondrial depolarization promotes calcium alternans: Mechanistic insights from a ventricular myocyte model." PLOS Computational Biology 17, no. 1 (2021): e1008624. http://dx.doi.org/10.1371/journal.pcbi.1008624.

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Mitochondria are vital organelles inside the cell and contribute to intracellular calcium (Ca2+) dynamics directly and indirectly via calcium exchange, ATP generation, and production of reactive oxygen species (ROS). Arrhythmogenic Ca2+ alternans in cardiac myocytes has been observed in experiments under abnormal mitochondrial depolarization. However, complex signaling pathways and Ca2+ cycling between mitochondria and cytosol make it difficult in experiments to reveal the underlying mechanisms of Ca2+ alternans under abnormal mitochondrial depolarization. In this study, we use a newly develop

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Wang, Guoqiang, Elisabeth Mémin, Ishwarya Murali, and Lawrence D. Gaspers. "The effect of chronic alcohol consumption on mitochondrial calcium handling in hepatocytes." Biochemical Journal 473, no. 21 (2016): 3903–21. http://dx.doi.org/10.1042/bcj20160255.

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The damage to liver mitochondria is universally observed in both humans and animal models after excessive alcohol consumption. Acute alcohol treatment has been shown to stimulate calcium (Ca2+) release from internal stores in hepatocytes. The resultant increase in cytosolic Ca2+ is expected to be accumulated by neighboring mitochondria, which could potentially lead to mitochondrial Ca2+ overload and injury. Our data indicate that total and free mitochondrial matrix Ca2+ levels are, indeed, elevated in hepatocytes isolated from alcohol-fed rats compared with their pair-fed control littermates.

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Ghosh, Sagnika, Writoban Basu Ball, Travis R. Madaris, et al. "An essential role for cardiolipin in the stability and function of the mitochondrial calcium uniporter." Proceedings of the National Academy of Sciences 117, no. 28 (2020): 16383–90. http://dx.doi.org/10.1073/pnas.2000640117.

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Calcium uptake by the mitochondrial calcium uniporter coordinates cytosolic signaling events with mitochondrial bioenergetics. During the past decade all protein components of the mitochondrial calcium uniporter have been identified, including MCU, the pore-forming subunit. However, the specific lipid requirements, if any, for the function and formation of this channel complex are currently not known. Here we utilize yeast, which lacks the mitochondrial calcium uniporter, as a model system to address this problem. We use heterologous expression to functionally reconstitute human uniporter mach

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Dikalov, Sergey I., Wei Li, Abdulrahman K. Doughan, Raul R. Blanco, and A. Maziar Zafari. "Mitochondrial reactive oxygen species and calcium uptake regulate activation of phagocytic NADPH oxidase." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 302, no. 10 (2012): R1134—R1142. http://dx.doi.org/10.1152/ajpregu.00842.2010.

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Production of superoxide (O2·−) by NADPH oxidases contributes to the development of hypertension and atherosclerosis. Factors responsible for activation of NADPH oxidases are not well understood; interestingly, cardiovascular disease is associated with both altered NADPH oxidase activity and age-associated mitochondrial dysfunction. We hypothesized that mitochondrial dysfunction may contribute to activation of NADPH oxidase. The effect of mitochondrial inhibitors on phagocytic NADPH oxidase in human lymphoblasts and whole blood was measured at the basal state and upon PKC-dependent stimulation

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Pallafacchina, Giorgia, Sofia Zanin, and Rosario Rizzuto. "Recent advances in the molecular mechanism of mitochondrial calcium uptake." F1000Research 7 (November 28, 2018): 1858. http://dx.doi.org/10.12688/f1000research.15723.1.

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In the last few decades, a large body of experimental evidence has highlighted the complex role for mitochondria in eukaryotic cells: they are not only the site of aerobic metabolism (thus providing most of the ATP supply for endergonic processes) but also a crucial checkpoint of cell death processes (both necrosis and apoptosis) and autophagy. For this purpose, mitochondria must receive and decode the wide variety of physiological and pathological stimuli impacting on the cell. The “old” notion that mitochondria possess a sophisticated machinery for accumulating and releasing Ca2+, the most c

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Babcock, Donner F., James Herrington, Paul C. Goodwin, Young Bae Park, and Bertil Hille. "Mitochondrial Participation in the Intracellular Ca2+ Network." Journal of Cell Biology 136, no. 4 (1997): 833–44. http://dx.doi.org/10.1083/jcb.136.4.833.

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Calcium can activate mitochondrial metabolism, and the possibility that mitochondrial Ca2+ uptake and extrusion modulate free cytosolic [Ca2+] (Cac) now has renewed interest. We use whole-cell and perforated patch clamp methods together with rapid local perfusion to introduce probes and inhibitors to rat chromaffin cells, to evoke Ca2+ entry, and to monitor Ca2+-activated currents that report near-surface [Ca2+]. We show that rapid recovery from elevations of Cac requires both the mitochondrial Ca2+ uniporter and the mitochondrial energization that drives Ca2+ uptake through it. Applying imagi

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