M R Duchen

Summary

Affiliation: University College London
Country: UK

Publications

  1. pmc Targeted polyphosphatase expression alters mitochondrial metabolism and inhibits calcium-dependent cell death
    Andrey Y Abramov
    Department of Physiology and Mitochondrial Biology Group, University College London, Gower Street, London WC1E 6BT, United Kingdom
    Proc Natl Acad Sci U S A 104:18091-6. 2007
  2. pmc Mitochondria and quality control defects in a mouse model of Gaucher disease--links to Parkinson's disease
    Laura D Osellame
    Department of Cell and Developmental Biology, University College London, London WC1E 6BT, UK
    Cell Metab 17:941-53. 2013
  3. pmc Cellular and molecular mechanisms of mitochondrial function
    Laura D Osellame
    Department of Cell and Developmental Biology, University College London, London WC1E 6BT, United Kingdom
    Best Pract Res Clin Endocrinol Metab 26:711-23. 2012
  4. pmc Mitochondria, calcium-dependent neuronal death and neurodegenerative disease
    Michael R Duchen
    Department of Cell and Developmental Biology, University College London, Gower Street, London, WC1E 6BT, UK
    Pflugers Arch 464:111-21. 2012
  5. ncbi request reprint Roles of mitochondria in human disease
    Michael R Duchen
    Department of Cell and Developmental Biology and Consortium for Mitochondrial Research, University College London, Gower Street, London WC1E 6BT, UK
    Essays Biochem 47:115-37. 2010
  6. ncbi request reprint Roles of mitochondria in health and disease
    Michael R Duchen
    Department of Physiology, University College London, London, UK
    Diabetes 53:S96-102. 2004
  7. ncbi request reprint Mitochondria in health and disease: perspectives on a new mitochondrial biology
    Michael R Duchen
    Department of Physiology and Mitochondrial Biology Group, University College London, Gower Street, London WC1E 6BT, UK
    Mol Aspects Med 25:365-451. 2004
  8. ncbi request reprint Mitochondria and Ca(2+)in cell physiology and pathophysiology
    M R Duchen
    Mitochondrial Biology Group and Life Sciences Imaging Consortium, Department of Physiology, University College London, Gower Street, London, WC1E 6BT, UK
    Cell Calcium 28:339-48. 2000
  9. pmc Mitochondria and calcium: from cell signalling to cell death
    M R Duchen
    Life Sciences Imaging Consortium and Mitochondrial Biology Group, Department of Physiology, University College London, Gower Street, London WC1E 6BT, UK
    J Physiol 529:57-68. 2000
  10. pmc Contributions of mitochondria to animal physiology: from homeostatic sensor to calcium signalling and cell death
    M R Duchen
    Department of Physiology, University College London, Gower Street, London WC1E 6BT, UK
    J Physiol 516:1-17. 1999

Detail Information

Publications73

  1. pmc Targeted polyphosphatase expression alters mitochondrial metabolism and inhibits calcium-dependent cell death
    Andrey Y Abramov
    Department of Physiology and Mitochondrial Biology Group, University College London, Gower Street, London WC1E 6BT, United Kingdom
    Proc Natl Acad Sci U S A 104:18091-6. 2007
    ..This confers protection against cell death, including that induced by beta-amyloid peptide, a pathogenic agent in Alzheimer's disease. These results demonstrate a crucial role played by polyP in mitochondrial function of mammalian cells...
  2. pmc Mitochondria and quality control defects in a mouse model of Gaucher disease--links to Parkinson's disease
    Laura D Osellame
    Department of Cell and Developmental Biology, University College London, London WC1E 6BT, UK
    Cell Metab 17:941-53. 2013
    ..These data provide conclusive evidence for mitochondrial dysfunction in GD and provide insight into the pathogenesis of PD and PD-GBA...
  3. pmc Cellular and molecular mechanisms of mitochondrial function
    Laura D Osellame
    Department of Cell and Developmental Biology, University College London, London WC1E 6BT, United Kingdom
    Best Pract Res Clin Endocrinol Metab 26:711-23. 2012
    ..Mitochondrial dysfunction is implicated in metabolic and age related disorders, neurodegenerative diseases and ischemic injury in heart and brain...
  4. pmc Mitochondria, calcium-dependent neuronal death and neurodegenerative disease
    Michael R Duchen
    Department of Cell and Developmental Biology, University College London, Gower Street, London, WC1E 6BT, UK
    Pflugers Arch 464:111-21. 2012
    ....
  5. ncbi request reprint Roles of mitochondria in human disease
    Michael R Duchen
    Department of Cell and Developmental Biology and Consortium for Mitochondrial Research, University College London, Gower Street, London WC1E 6BT, UK
    Essays Biochem 47:115-37. 2010
    ....
  6. ncbi request reprint Roles of mitochondria in health and disease
    Michael R Duchen
    Department of Physiology, University College London, London, UK
    Diabetes 53:S96-102. 2004
    ..The calcium increase mediated by NMDA receptor activation is thus associated with nitric oxide generation, and the combination leads to the collapse of mitochondrial membrane potential followed by cell death...
  7. ncbi request reprint Mitochondria in health and disease: perspectives on a new mitochondrial biology
    Michael R Duchen
    Department of Physiology and Mitochondrial Biology Group, University College London, Gower Street, London WC1E 6BT, UK
    Mol Aspects Med 25:365-451. 2004
    ....
  8. ncbi request reprint Mitochondria and Ca(2+)in cell physiology and pathophysiology
    M R Duchen
    Mitochondrial Biology Group and Life Sciences Imaging Consortium, Department of Physiology, University College London, Gower Street, London, WC1E 6BT, UK
    Cell Calcium 28:339-48. 2000
    ....
  9. pmc Mitochondria and calcium: from cell signalling to cell death
    M R Duchen
    Life Sciences Imaging Consortium and Mitochondrial Biology Group, Department of Physiology, University College London, Gower Street, London WC1E 6BT, UK
    J Physiol 529:57-68. 2000
    ..Mitochondrial Ca2+ uptake in combination with NO production triggers the collapse of mitochondrial membrane potential, culminating in delayed cell death...
  10. pmc Contributions of mitochondria to animal physiology: from homeostatic sensor to calcium signalling and cell death
    M R Duchen
    Department of Physiology, University College London, Gower Street, London WC1E 6BT, UK
    J Physiol 516:1-17. 1999
    ..This review looks at recent developments in these rapidly evolving areas of cell physiology in an attempt to draw together disparate areas of research into a common theme...
  11. pmc Transient mitochondrial depolarizations reflect focal sarcoplasmic reticular calcium release in single rat cardiomyocytes
    M R Duchen
    Department of Physiology, University College London, London WC1E 6BT, United Kingdom
    J Cell Biol 142:975-88. 1998
    ....
  12. pmc Excitotoxic mitochondrial depolarisation requires both calcium and nitric oxide in rat hippocampal neurons
    J Keelan
    Department of Physiology, University College London, Gower Street, London WC1E 6BT, UK
    J Physiol 520:797-813. 1999
    ..These data suggest that [Ca2+]c and nitric oxide act synergistically to cause mitochondrial dysfunction and impaired [Ca2+]c homeostasis during glutamate toxicity...
  13. pmc Glutamate-induced mitochondrial depolarisation and perturbation of calcium homeostasis in cultured rat hippocampal neurones
    O Vergun
    Department of Physiology, University College London, Gower Street, London WC1E 6BT, UK
    J Physiol 519:451-66. 1999
    ..These data suggest that mitochondrial dysfunction plays a major role in the deregulation of [Ca2+]i associated with glutamate toxicity...
  14. ncbi request reprint Beta-amyloid peptides induce mitochondrial dysfunction and oxidative stress in astrocytes and death of neurons through activation of NADPH oxidase
    Andrey Y Abramov
    Mitochondrial Biology Group, Department of Physiology, University College London, London WC1E 6BT, United Kingdom
    J Neurosci 24:565-75. 2004
    ....
  15. pmc PINK1-associated Parkinson's disease is caused by neuronal vulnerability to calcium-induced cell death
    Sonia Gandhi
    Department of Molecular Neuroscience, Institute of Neurology, Queen Square, London, UK
    Mol Cell 33:627-38. 2009
    ..Our findings propose a mechanism by which PINK1 dysfunction renders neurons vulnerable to cell death...
  16. pmc Albumin uptake in OK cells exposed to rotenone: a model for studying the effects of mitochondrial dysfunction on endocytosis in the proximal tubule?
    A M Hall
    Centre for Nephrology, University of London, London, UK
    Nephron Physiol 115:p9-p19. 2010
    ..As the mechanism that couples mitochondrial dysfunction to impaired PT low-molecular weight protein uptake is unknown, we investigated the effect of respiratory chain (RC) inhibitors on endocytosis of FITC-albumin in PT-derived OK cells...
  17. pmc Exploration of the role of reactive oxygen species in glutamate neurotoxicity in rat hippocampal neurones in culture
    O Vergun
    Department of Physiology, University College London, Gower Street, London WC1E 6BT, UK
    J Physiol 531:147-63. 2001
    ..The data obtained suggest that antioxidants exert their protective effect against glutamate-induced neuronal death through steps downstream of a sustained increase in [Ca2+]c associated with the collapse of Deltapsi(m)...
  18. ncbi request reprint Expression and modulation of an NADPH oxidase in mammalian astrocytes
    Andrey Y Abramov
    Department of Physiology, University College London, London WC1E 6BT, United Kingdom
    J Neurosci 25:9176-84. 2005
    ..The astrocytic NADPH oxidase is likely to play important roles in CNS physiology and pathology...
  19. ncbi request reprint Changes in intracellular calcium and glutathione in astrocytes as the primary mechanism of amyloid neurotoxicity
    Andrey Y Abramov
    Mitochondrial Biology Group, Department of Physiology, University College London, London WC1E 6BT, United Kingdom
    J Neurosci 23:5088-95. 2003
    ..Thus, astrocytes appear to be the primary target of betaA, whereas the neurotoxicity reflects the neuronal dependence on astrocytes for antioxidant support...
  20. ncbi request reprint Imaging mitochondrial function in intact cells
    Michael R Duchen
    Life Sciences Imaging Cooperative and Mitochondrial Biology Group, Department of Physiology, University College London, London WC1E 6BT, United Kingdom
    Methods Enzymol 361:353-89. 2003
  21. pmc The role of an astrocytic NADPH oxidase in the neurotoxicity of amyloid beta peptides
    Andrey Y Abramov
    University College London Department of Physiology Gower Street, London WC1E 6BT, UK
    Philos Trans R Soc Lond B Biol Sci 360:2309-14. 2005
    ..Thus, by raising [Ca2+]c in astrocytes, Abeta activates NOX, generating oxidative stress that is transmitted to neurons, causing neuronal death...
  22. ncbi request reprint Mitochondrial oxidative stress and cell death in astrocytes--requirement for stored Ca2+ and sustained opening of the permeability transition pore
    Jake Jacobson
    Department of Physiology, University College London, London, WC1E 6BT, UK
    J Cell Sci 115:1175-88. 2002
    ..The amplification of oxidative stress and Ca2+ loading culminates in opening of the mPTP and necrotic cell death in primary brain cells...
  23. doi request reprint IF1, the endogenous regulator of the F(1)F(o)-ATPsynthase, defines mitochondrial volume fraction in HeLa cells by regulating autophagy
    Michelangelo Campanella
    Department of Cell and Developmental Biology, University College London, UK
    Biochim Biophys Acta 1787:393-401. 2009
    ..Variations in IF1 expression level may therefore play a significant role in defining both resting rates of ROS generation and cellular mitochondrial content...
  24. pmc Hypoxia-induced catecholamine secretion in isolated newborn rat adrenal chromaffin cells is mimicked by inhibition of mitochondrial respiration
    M H Mojet
    Department of Physiology, University College London, UK
    J Physiol 504:175-89. 1997
    ..6. These data indicate that hypoxia-induced catecholamine secretion in the newborn adrenal medulla is mediated by reversible inhibition of mitochondrial respiration, leading to an increase in [Ca2+]i and catecholamine secretion...
  25. doi request reprint Expression of mutant SOD1 in astrocytes induces functional deficits in motoneuron mitochondria
    Lynsey G Bilsland
    Sobell Department of Movement Disorders and Motor Neuroscience, Institute of Neurology, Queen Square, London, UK
    J Neurochem 107:1271-83. 2008
    ..These early deficits in mitochondrial function induced by surrounding astrocytes may increase the vulnerability of motoneurons to other neurotoxic mechanisms involved in ALS pathogenesis...
  26. ncbi request reprint Quantitative imaging of glutathione in hippocampal neurons and glia in culture using monochlorobimane
    J Keelan
    Department of Physiology, University College London, Gower Street, London WC1N 6BT, United Kingdom
    J Neurosci Res 66:873-84. 2001
    ..Such neurotoxicity was independent of the endogenous glutamate and nitric oxide synthase, suggesting that it is not due to secondary excitotoxicity...
  27. ncbi request reprint Mitochondria as targets for nitric oxide-induced protection during simulated ischemia and reoxygenation in isolated neonatal cardiomyocytes
    R D Rakhit
    Departments of Cardiology, Kings College London, St Thomas' Hospital, University College London, UK
    Circulation 103:2617-23. 2001
    ..The demonstrated reduction in mitochondrial Ca(2+) uptake possibly reduces cytosolic Ca(2+) overload, providing a likely mechanism for NO-induced protection...
  28. doi request reprint Mitochondria modulate the spatio-temporal properties of intra- and intercellular Ca2+ signals in cochlear supporting cells
    Zoë F Mann
    UCL Ear Institute, 332 Gray s Inn Road, London WC1X 8EE, UK Department of Cell and Developmental Biology, University College London, Gower Street, London WC1E 6BT, UK
    Cell Calcium 46:136-46. 2009
    ..Thus, mitochondria function as spatial Ca2+ buffers during agonist-evoked [Ca2+](cyt) signalling in cochlear supporting cells and play a significant role in regulating the spatio-temporal properties of intercellular Ca2+ waves...
  29. ncbi request reprint Actions of ionomycin, 4-BrA23187 and a novel electrogenic Ca2+ ionophore on mitochondria in intact cells
    Andrey Y Abramov
    Department of Physiology and Mitochondrial Biology Group, University College London, Gower Street, London WC1E 6BT, UK
    Cell Calcium 33:101-12. 2003
    ..We suggest that ferutinin may provide a very valuable tool to promote mitochondrial calcium overload experimentally and to promote calcium-dependent opening of the mPTP...
  30. pmc Substrate-dependent changes in mitochondrial function, intracellular free calcium concentration and membrane channels in pancreatic beta-cells
    M R Duchen
    Department of Physiology, University College London, U K
    Biochem J 294:35-42. 1993
    ..These data are consistent with a central role for mitochondrial oxidative phosphorylation in coupling changes in glucose concentration with the secretion of insulin...
  31. ncbi request reprint Interrelationships between astrocyte function, oxidative stress and antioxidant status within the central nervous system
    S Peuchen
    Department of Neurochemistry, Institute of Neurology, London, U K
    Prog Neurobiol 52:261-81. 1997
    ..The glutathione antioxidant system will be the focus of attention, since astrocytes have an enormous capacity for, and efficiency built into this particular system...
  32. doi request reprint Mitochondria: the hub of cellular Ca2+ signaling
    Gyorgy Szabadkai
    Department of Physiology, Mitochondrial Biology Group, University College London, London, United Kingdom
    Physiology (Bethesda) 23:84-94. 2008
    ..We here review the ways in which this system provides integrity and flexibility for the cell to cope with the countless demands throughout its life cycle and discuss briefly the mechanisms through which it can also drive cell death...
  33. ncbi request reprint Mechanisms underlying the loss of mitochondrial membrane potential in glutamate excitotoxicity
    Andrey Y Abramov
    Department of Physiology, University College London, Gower Street, London WC1E 6BT, UK
    Biochim Biophys Acta 1777:953-64. 2008
    ..Thus, mitochondrial depolarisation represents two consecutive but distinct processes driving cell death, the first of which is reversible while the second is not...
  34. ncbi request reprint Endothelial mitochondria: contributing to vascular function and disease
    Sean M Davidson
    The Hatter Cardiovascular Institute, Department of Medicine, Royal Free and University College Medical School, London, United Kingdom
    Circ Res 100:1128-41. 2007
    ....
  35. doi request reprint Mitochondria mediated cell death in diabetes
    Gyorgy Szabadkai
    Department of Cell and Developmental Biology, Mitochondrial Biology Group, University College London, Gower Street, WC1E 6BT London, UK
    Apoptosis 14:1405-23. 2009
    ..We summarize the main findings supporting such a pivotal role of mitochondria in beta-cell death in the context of current trends in diabetes research...
  36. pmc Multiphoton imaging reveals differences in mitochondrial function between nephron segments
    Andrew M Hall
    Department of Cell and Developmental Biology, University College London, London WC1E 6BT, UK
    J Am Soc Nephrol 20:1293-302. 2009
    ..In summary, there are axial differences in mitochondrial function along the nephron, which may contribute to the pattern and pathophysiology of some forms of renal injury...
  37. doi request reprint IF(1): setting the pace of the F(1)F(o)-ATP synthase
    Michelangelo Campanella
    Department of Cell and Developmental Biology, University College London, UK
    Trends Biochem Sci 34:343-50. 2009
    ..Emerging research suggests that IF(1) has a wider ranging impact on mitochondrial structure and function than previously thought...
  38. doi request reprint Impaired mitochondrial bioenergetics determines glutamate-induced delayed calcium deregulation in neurons
    Andrey Y Abramov
    Department of Molecular Neuroscience, UCL Institute of Neurology, Queen Square, London WC1N 3 BG, UK
    Biochim Biophys Acta 1800:297-304. 2010
    ..Exposure of neurons to toxic glutamate concentrations causes an initial transient increase in [Ca(2+)](c) followed by a delayed increase commonly termed delayed [Ca(2+)](c) deregulation (DCD)...
  39. pmc Mechanism of neurodegeneration of neurons with mitochondrial DNA mutations
    Andrey Y Abramov
    Department of Molecular Neuroscience, UCL Institute of Neurology, Queen Square, London, WC1N 3BG, UK
    Brain 133:797-807. 2010
    ..Thus, in neurons with a severe mutation of complex I, the maintenance of a high potential by F(1)F(o) ATPase activity combined with an impaired respiratory chain causes oxidative stress which promotes cell death...
  40. ncbi request reprint Three distinct mechanisms generate oxygen free radicals in neurons and contribute to cell death during anoxia and reoxygenation
    Andrey Y Abramov
    Department of Physiology, University College London, London WC1E 6BT, United Kingdom
    J Neurosci 27:1129-38. 2007
    ..Inhibition of either the NADPH oxidase or XO was significantly neuroprotective. Thus, oxidative stress contributes to cell death over and above the injury attributable to energy deprivation...
  41. ncbi request reprint Calcium microdomains and oxidative stress
    Sean M Davidson
    The Hatter Cardiovascular Institute, Royal Free and University College Medical School, London, Department of Medicine, 67 Chenies Mews, London, UK
    Cell Calcium 40:561-74. 2006
    ....
  42. ncbi request reprint Calcium signals induced by amyloid beta peptide and their consequences in neurons and astrocytes in culture
    Andrey Y Abramov
    Department of Physiology, University College London, Gower Street WC1E 6BT, London, UK
    Biochim Biophys Acta 1742:81-7. 2004
    ..These data suggest that Abeta causes Ca(2+)-dependent oxidative stress by activating an astrocytic NADPH oxidase, and that neuronal death follows through a failure of antioxidant support...
  43. ncbi request reprint Interplay between mitochondria and cellular calcium signalling
    Jake Jacobson
    Department of Physiology, University College London, London, UK
    Mol Cell Biochem 256:209-18. 2004
    ....
  44. ncbi request reprint Induction of mitochondrial oxidative stress in astrocytes by nitric oxide precedes disruption of energy metabolism
    Jake Jacobson
    Miriam Marks Division of Neurochemistry, Institute of Neurology, Department of Biology, University College London, London, UK
    J Neurochem 95:388-95. 2005
    ..These data suggest that partial ETC inhibition by NO may initially cause oxidative stress rather than ATP depletion, and this may subsequently induce irreversible changes in ETC function providing the basis for a cycle of damage...
  45. ncbi request reprint Toxicity of amyloid beta peptide: tales of calcium, mitochondria, and oxidative stress
    Laura Canevari
    Division of Neurochemistry, Institute of Neurology, Queen Square, London WC1N 3BG, United Kingdom
    Neurochem Res 29:637-50. 2004
    ..Studies in vitro also show alterations in cellular calcium signaling. We consider the mechanisms proposed to mediate cell injury and explore evidence to indicate which of these many changes in function are primary and which secondary...
  46. doi request reprint CLIC1 function is required for beta-amyloid-induced generation of reactive oxygen species by microglia
    Rosemary H Milton
    Department of Physiology, University College London, London, United Kingdom
    J Neurosci 28:11488-99. 2008
    ....
  47. ncbi request reprint Effects of NO on mitochondrial function in cardiomyocytes: Pathophysiological relevance
    Sean M Davidson
    The Hatter Cardiovascular Institute, Department of Medicine, Royal Free and University College Medical School, 67 Chenies Mews, University College Hospital, London WC1E 6HX, United Kingdom
    Cardiovasc Res 71:10-21. 2006
    ....
  48. ncbi request reprint Intracellular distribution of the fluorescent dye nonyl acridine orange responds to the mitochondrial membrane potential: implications for assays of cardiolipin and mitochondrial mass
    Jake Jacobson
    Department of Molecular Pathogenesis, Institute of Neurology, National Hospital for Neurology and Neurosurgery, London, UK
    J Neurochem 82:224-33. 2002
    ..These observations demonstrate that loading and retention of NAO is dependant upon membrane potential, and that the dye cannot be used as an assay of either cardiolipin or mitochondrial mass in living cells...
  49. pmc IF1 limits the apoptotic-signalling cascade by preventing mitochondrial remodelling
    D Faccenda
    Department of Comparative Biomedical Sciences, The Royal Veterinary College, University of London, London, UK
    Cell Death Differ 20:686-97. 2013
    ..These data suggest that IF1 is an antiapoptotic and potentially tumorigenic factor and may be a valuable predictor of responsiveness to chemotherapy...
  50. ncbi request reprint Assessing mitochondrial potential, calcium, and redox state in isolated mammalian cells using confocal microscopy
    Sean M Davidson
    The Hatter Institute and Centre for Cardiology, University College London, United Kingdom
    Methods Mol Biol 372:421-30. 2007
    ..We demonstrate how these parameters can be analyzed in parallel using the emission spectra "fingerprinting" method even when emission spectra overlap...
  51. ncbi request reprint Altered mechanical properties and intracellular calcium signaling in cardiomyocytes from annexin 6 null-mutant mice
    Guojie Song
    Division of Cell Biology, Institute of Ophthalmology, University College London, London EC1V 9EL, UK
    FASEB J 16:622-4. 2002
    ..In light of published findings showing annexin 6 to be down-regulated in end-stage heart failure, these results are consistent with a role for annexin 6 as a negative inotropic factor in the regulation of cardiomyocyte mechanics...
  52. pmc Deletion of the von Hippel-Lindau gene in pancreatic beta cells impairs glucose homeostasis in mice
    James Cantley
    Centre for Diabetes and Endocrinology, Faculty of Medicine, Rayne Institute, University College London, London, UK
    J Clin Invest 119:125-35. 2009
    ..These data suggest that VHL/HIF oxygen-sensing mechanisms play a critical role in glucose homeostasis and that activation of this pathway in response to decreased islet oxygenation may contribute to beta cell dysfunction...
  53. ncbi request reprint Beta-amyloid fragment 25-35 causes mitochondrial dysfunction in primary cortical neurons
    C S Casley
    Division of Neurochemistry, Institute of Neurology, University College London, Queen Square, London WC1N 3BG, United Kingdom
    Neurobiol Dis 10:258-67. 2002
    ..In astrocytes mitochondrial impairment was confined to complex I inhibition, whereas in neurons a generalized loss of mitochondria was seen...
  54. doi request reprint Regulation of mitochondrial structure and function by the F1Fo-ATPase inhibitor protein, IF1
    Michelangelo Campanella
    Department of Physiology, University College London, Gower Street, London WC1E 6BT, UK
    Cell Metab 8:13-25. 2008
    ..Thus, IF(1) regulates mitochondrial function and structure under both physiological and pathological conditions...
  55. ncbi request reprint Signalling via the reperfusion injury signalling kinase (RISK) pathway links closure of the mitochondrial permeability transition pore to cardioprotection
    Sean M Davidson
    The Hatter Cardiovascular Institute, University College London Hospitals and Medical School, London, UK
    Int J Biochem Cell Biol 38:414-9. 2006
    ..These results indicate that activation of the PI3K-Akt pro-survival kinase pathway inhibits opening of the mPTP, and demonstrate an important link between the survival kinases and the mPTP...
  56. pmc The large-conductance Ca2+-activated K+ channel is essential for innate immunity
    Jatinder Ahluwalia
    Department of Medicine University College London, Gower Street, London WC1E 6BT, UK
    Nature 427:853-8. 2004
    ..Remarkably, microbial killing and digestion were abolished when the BK(Ca) channel was blocked, revealing an essential and unexpected function for this K+ channel in the microbicidal process...
  57. pmc PINK1 is necessary for long term survival and mitochondrial function in human dopaminergic neurons
    Alison Wood-Kaczmar
    Department of Molecular Neuroscience, Institute of Neurology, London, United Kingdom
    PLoS ONE 3:e2455. 2008
    ..The phenotypic effects of PINK1 loss-of-function described here in mammalian neurons provides mechanistic insight into the age-related degeneration of nigral dopaminergic neurons seen in PD...
  58. doi request reprint Renal function and mitochondrial cytopathy (MC): more questions than answers?
    A M Hall
    Department of Physiology, University College London, London, UK
    QJM 101:755-66. 2008
    ....
  59. doi request reprint The intracellular localization and function of the ATP-sensitive K+ channel subunit Kir6.1
    Keat Eng Ng
    Deparment of Medicine, The Rayne Institute, University College London, Room 107, University Street, London, WC1E 6JF, UK
    J Membr Biol 234:137-47. 2010
    ..This study suggests that Kir6.1 is located in the endoplasmic reticulum and plays a role in modifying Ca2+ release from intracellular stores...
  60. pmc Extracellular growth factors and mitogens cooperate to drive mitochondrial biogenesis
    Pedro Echave
    MRC Laboratory for Molecular Cell Biology, The Cancer Institute, University College London, London, UK
    J Cell Sci 122:4516-25. 2009
    ..This separation of the pathways that drive mitochondrial biogenesis and cell growth provides a mechanism for the modulation of mitochondrial density according to the metabolic requirements of the cell...
  61. ncbi request reprint Preconditioning protects by inhibiting the mitochondrial permeability transition
    Derek J Hausenloy
    The Hatter Institute and Centre for Cardiology, University College London Hospitals and Medical School, Grafton Way, London WC1E 6DB, UK
    Am J Physiol Heart Circ Physiol 287:H841-9. 2004
    ..In conclusion, preconditioning protects the myocardium by reducing the probability of the mPT, which normally occurs during ischemia-reperfusion in response to oxidative stress...
  62. ncbi request reprint FCCP is cardioprotective at concentrations that cause mitochondrial oxidation without detectable depolarisation
    Jonathan P Brennan
    Cardiac Physiology Cardiovascular Division, King s College London, SE1 7EH, UK
    Cardiovasc Res 72:322-30. 2006
    ..Here we define the mitochondrial responses to increasing concentrations of FCCP and also to explore the equivalence of the cardioprotective doses of diazoxide...
  63. ncbi request reprint Mitochondrial uncoupling, with low concentration FCCP, induces ROS-dependent cardioprotection independent of KATP channel activation
    Jonathan P Brennan
    Cardiac Physiology Cardiovascular Division, The Rayne Institute, St Thomas Hospital, King s College London, SE1 7EH, UK
    Cardiovasc Res 72:313-21. 2006
    ....
  64. ncbi request reprint Mitochondria, Ca2+ and neurodegenerative disease
    Charles Krieger
    School of Kinesiology, Simon Fraser University, Burnaby, BC, Canada
    Eur J Pharmacol 447:177-88. 2002
    ..Evidence is also accumulating to suggest that more subtle alterations in mitochondrial function may serve as predisposing factors in the pathogenesis of a number of neurodegenerative disorders...
  65. ncbi request reprint IL-6 induces PI 3-kinase and nitric oxide-dependent protection and preserves mitochondrial function in cardiomyocytes
    Nicola Smart
    Cardiovascular Division, King s College London School of Medicine, Department of Cardiology, The Rayne Institute, St Thomas Hospital, Lambeth Palace Road, London SE1 7EH, UK
    Cardiovasc Res 69:164-77. 2006
    ..On the other hand, IL-6 activates signalling pathways which mediate delayed ischemic preconditioning. We have therefore studied the cellular mechanisms of IL-6-induced cardioprotection...
  66. ncbi request reprint Inhibiting mitochondrial permeability transition pore opening at reperfusion protects against ischaemia-reperfusion injury
    Derek J Hausenloy
    The Hatter Institute and Centre for Cardiology, University College London Hospitals and Medical School, Grafton Way, WC1E 6DB London, UK
    Cardiovasc Res 60:617-25. 2003
    ..We hypothesised that the novel immunosuppressant, sanglifehrin-A (SFA), given at the time of reperfusion, protects the myocardium from ischaemia-reperfusion injury, by suppressing mPTP opening...
  67. ncbi request reprint Mitochondrial permeability transition pore as a target for cardioprotection in the human heart
    Selvaraj Shanmuganathan
    Hatter Institute and Center for Cardiology, University College London Hospitals and Medical School, Grafton Way, London WC1E 6DB, UK
    Am J Physiol Heart Circ Physiol 289:H237-42. 2005
    ..01). We report that suppressing mPTP opening at the onset of reoxygenation protects human myocardium against lethal hypoxia-reoxygenation injury. This suggests that, in the human heart, the mPTP is a viable target for cardioprotection...
  68. ncbi request reprint Flirting in little space: the ER/mitochondria Ca2+ liaison
    Rosario Rizzuto
    Department of Experimental and Diagnostic Medicine, Section of General Pathology, University of Ferrara, Italy
    Sci STKE 2004:re1. 2004
    ....
  69. ncbi request reprint Effects of beauvericin on the metabolic state and ionic homeostasis of ventricular myocytes of the guinea pig
    Katerina Kouri
    Department of Pharmacology and Toxicology, University of Vienna, Althanstrasse 14, 1090 Vienna, Austria
    Chem Res Toxicol 18:1661-8. 2005
    ....
  70. ncbi request reprint Prostaglandin F2alpha potentiates the calcium dependent activation of mitochondrial metabolism in luteal cells
    János G Pitter
    Laboratory of Cellular and Molecular Physiology, Department of Physiology, Semmelweis University and Hungarian Academy of Sciences, P O Box 259, H 1444 Budapest, Hungary
    Cell Calcium 37:35-44. 2005
    ....
  71. ncbi request reprint Regulation of redox metabolism in the mouse oocyte and embryo
    Remi Dumollard
    Laboratoire de Biologie du Développement UMR 7009 CNRS Paris VI, Observatoire, Station Zoologique, Villefranche sur Mer, France
    Development 134:455-65. 2007
    ..Remarkably, we also found that the oxidant action of pyruvate impairs development, demonstrating the fundamental importance of redox state on early development...
  72. ncbi request reprint Mitochondrial ND5 gene variation associated with encephalomyopathy and mitochondrial ATP consumption
    Matthew McKenzie
    Department of Biochemistry, La Trobe University, Melbourne 3086, Australia
    J Biol Chem 282:36845-52. 2007
    ..These data suggest that in response to impaired respiration due to the mtDNA mutation, mitochondria consume ATP to maintain Deltapsim, representing a potential pathophysiological mechanism in human mitochondrial disease...