Research Topics
| M R DuchenSummaryAffiliation: University College London Country: UK Publications
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Detail Information
Publications
Targeted polyphosphatase expression alters mitochondrial metabolism and inhibits calcium-dependent cell deathAndrey 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...- Mitochondria and Ca(2+)in cell physiology and pathophysiologyM 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.... - Roles of mitochondria in health and diseaseMichael 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... - Roles of mitochondria in human diseaseMichael 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.... - Mitochondria and calcium: from cell signalling to cell deathM 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... - Contributions of mitochondria to animal physiology: from homeostatic sensor to calcium signalling and cell deathM 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... - Transient mitochondrial depolarizations reflect focal sarcoplasmic reticular calcium release in single rat cardiomyocytesM R Duchen
Department of Physiology, University College London, London WC1E 6BT, United Kingdom
J Cell Biol 142:975-88. 1998.... - Mitochondria in health and disease: perspectives on a new mitochondrial biologyMichael 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.... - Glutamate-induced mitochondrial depolarisation and perturbation of calcium homeostasis in cultured rat hippocampal neuronesO 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... - Excitotoxic mitochondrial depolarisation requires both calcium and nitric oxide in rat hippocampal neuronsJ 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... - Beta-amyloid peptides induce mitochondrial dysfunction and oxidative stress in astrocytes and death of neurons through activation of NADPH oxidaseAndrey Y Abramov
Mitochondrial Biology Group, Department of Physiology, University College London, London WC1E 6BT, United Kingdom
J Neurosci 24:565-75. 2004.... - PINK1-associated Parkinson's disease is caused by neuronal vulnerability to calcium-induced cell deathSonia 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... - Expression and modulation of an NADPH oxidase in mammalian astrocytesAndrey 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... - Changes in intracellular calcium and glutathione in astrocytes as the primary mechanism of amyloid neurotoxicityAndrey 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... - Imaging mitochondrial function in intact cellsMichael 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 - Exploration of the role of reactive oxygen species in glutamate neurotoxicity in rat hippocampal neurones in cultureO 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)... - 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... - The role of an astrocytic NADPH oxidase in the neurotoxicity of amyloid beta peptidesAndrey 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... - IF1, the endogenous regulator of the F(1)F(o)-ATPsynthase, defines mitochondrial volume fraction in HeLa cells by regulating autophagyMichelangelo 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... - Mitochondrial oxidative stress and cell death in astrocytes--requirement for stored Ca2+ and sustained opening of the permeability transition poreJake 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... - Hypoxia-induced catecholamine secretion in isolated newborn rat adrenal chromaffin cells is mimicked by inhibition of mitochondrial respirationM 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... - Expression of mutant SOD1 in astrocytes induces functional deficits in motoneuron mitochondriaLynsey 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... - Mitochondria as targets for nitric oxide-induced protection during simulated ischemia and reoxygenation in isolated neonatal cardiomyocytesR 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... - Actions of ionomycin, 4-BrA23187 and a novel electrogenic Ca2+ ionophore on mitochondria in intact cellsAndrey 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... - Mitochondria modulate the spatio-temporal properties of intra- and intercellular Ca2+ signals in cochlear supporting cellsZoë 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... - Substrate-dependent changes in mitochondrial function, intracellular free calcium concentration and membrane channels in pancreatic beta-cellsM 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... - Interrelationships between astrocyte function, oxidative stress and antioxidant status within the central nervous systemS 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... - Effects of NO on mitochondrial function in cardiomyocytes: Pathophysiological relevanceSean 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.... - Calcium microdomains and oxidative stressSean 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.... - Three distinct mechanisms generate oxygen free radicals in neurons and contribute to cell death during anoxia and reoxygenationAndrey 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... - Endothelial mitochondria: contributing to vascular function and diseaseSean 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.... - Mitochondria: the hub of cellular Ca2+ signalingGyorgy 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... - Mechanisms underlying the loss of mitochondrial membrane potential in glutamate excitotoxicityAndrey 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... - IF(1): setting the pace of the F(1)F(o)-ATP synthaseMichelangelo 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... - CLIC1 function is required for beta-amyloid-induced generation of reactive oxygen species by microgliaRosemary H Milton
Department of Physiology, University College London, London, United Kingdom
J Neurosci 28:11488-99. 2008.... - Mechanism of neurodegeneration of neurons with mitochondrial DNA mutationsAndrey 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... - Mitochondria mediated cell death in diabetesGyorgy 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... - Impaired mitochondrial bioenergetics determines glutamate-induced delayed calcium deregulation in neuronsAndrey 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)... - Toxicity of amyloid beta peptide: tales of calcium, mitochondria, and oxidative stressLaura 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... - Calcium signals induced by amyloid beta peptide and their consequences in neurons and astrocytes in cultureAndrey 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... - Interplay between mitochondria and cellular calcium signallingJake Jacobson
Department of Physiology, University College London, London, UK
Mol Cell Biochem 256:209-18. 2004.... - Induction of mitochondrial oxidative stress in astrocytes by nitric oxide precedes disruption of energy metabolismJake 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... - Multiphoton imaging reveals differences in mitochondrial function between nephron segmentsAndrew 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... - Intracellular distribution of the fluorescent dye nonyl acridine orange responds to the mitochondrial membrane potential: implications for assays of cardiolipin and mitochondrial massJake 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... - Beta-amyloid fragment 25-35 causes mitochondrial dysfunction in primary cortical neuronsC 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... - Altered mechanical properties and intracellular calcium signaling in cardiomyocytes from annexin 6 null-mutant miceGuojie 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... - Deletion of the von Hippel-Lindau gene in pancreatic beta cells impairs glucose homeostasis in miceJames 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... - Assessing mitochondrial potential, calcium, and redox state in isolated mammalian cells using confocal microscopySean 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... - Quantitative imaging of glutathione in hippocampal neurons and glia in culture using monochlorobimaneJ 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... - The large-conductance Ca2+-activated K+ channel is essential for innate immunityJatinder 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... - PINK1 is necessary for long term survival and mitochondrial function in human dopaminergic neuronsAlison 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... - Regulation of mitochondrial structure and function by the F1Fo-ATPase inhibitor protein, IF1Michelangelo 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... - Signalling via the reperfusion injury signalling kinase (RISK) pathway links closure of the mitochondrial permeability transition pore to cardioprotectionSean 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... - 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.... - The intracellular localization and function of the ATP-sensitive K+ channel subunit Kir6.1Keat 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... - Extracellular growth factors and mitogens cooperate to drive mitochondrial biogenesisPedro 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... - Preconditioning protects by inhibiting the mitochondrial permeability transitionDerek 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... - Mitochondrial uncoupling, with low concentration FCCP, induces ROS-dependent cardioprotection independent of KATP channel activationJonathan 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..This cardioprotection is not mediated via the depletion of cellular ATP or mitochondrial K(ATP) channel activation... - FCCP is cardioprotective at concentrations that cause mitochondrial oxidation without detectable depolarisationJonathan P Brennan
Cardiac Physiology (Cardiovascular Division, King's College London, SE1 7EH, UK
Cardiovasc Res 72:322-30. 2006..This establishes the principle that mild mitochondrial uncoupling activates a protective mechanism. Diazoxide did not cause mitochondrial oxidation or mitochondrial depolarisation, suggesting it induces protection via another mechanism... - Mitochondria, Ca2+ and neurodegenerative diseaseCharles 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... - Regulation of redox metabolism in the mouse oocyte and embryoRemi 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... - IL-6 induces PI 3-kinase and nitric oxide-dependent protection and preserves mitochondrial function in cardiomyocytesNicola 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.... - Inhibiting mitochondrial permeability transition pore opening at reperfusion protects against ischaemia-reperfusion injuryDerek 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..001). CONCLUSIONS: Inhibiting mPTP opening during the first few minutes of reperfusion, using sanglifehrin-A, limits infarct size and protects myocytes from oxidative stress... - Flirting in little space: the ER/mitochondria Ca2+ liaisonRosario Rizzuto
Department of Experimental and Diagnostic Medicine, Section of General Pathology, University of Ferrara, Italy
Sci STKE 2004:re1. 2004.... - Mitochondrial permeability transition pore as a target for cardioprotection in the human heartSelvaraj 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... - Effects of beauvericin on the metabolic state and ionic homeostasis of ventricular myocytes of the guinea pigKaterina Kouri
Department of Pharmacology and Toxicology, University of Vienna, Althanstrasse 14, 1090 Vienna, Austria
Chem Res Toxicol 18:1661-8. 2005.... - Mitochondrial ND5 gene variation associated with encephalomyopathy and mitochondrial ATP consumptionMatthew 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...