Complex I disorders: causes, mechanisms, and development of treatment strategies at the cellular level. (Q37785516)

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13 February 2020

title

Complex I disorders: causes, mechanisms, and development of treatment strategies at the cellular level (English)

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13 February 2020

4

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13 February 2020

Peter H Willems

6

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13 February 2020

author name string

Federica Valsecchi

1

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13 February 2020

Werner J H Koopman

2

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13 February 2020

Ganesh R Manjeri

3

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13 February 2020

Jan A M Smeitink

5

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13 February 2020

language of work or name

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1 January 2010

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Developmental Disabilities Research Reviews

13 February 2020

published in

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13 February 2020

volume

16

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issue

2

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13 February 2020

page(s)

175-182

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Mitochondria in health and disease: perspectives on a new mitochondrial biology

13 February 2020

cites work

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NDUFS6 mutations are a novel cause of lethal neonatal mitochondrial complex I deficiency

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Calcium and ATP handling in human NADH:ubiquinone oxidoreductase deficiency

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Superoxide production is inversely related to complex I activity in inherited complex I deficiency.

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Decreased agonist-stimulated mitochondrial ATP production caused by a pathological reduction in endoplasmic reticulum calcium content in human complex I deficiency

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Mitochondria-targeted plastoquinone derivatives as tools to interrupt execution of the aging program. 3. Inhibitory effect of SkQ1 on tumor development from p53-deficient cells.

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The on-off switches of the mitochondrial uncoupling proteins

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Mitochondria-targeted plastoquinone derivatives as tools to interrupt execution of the aging program. 2. Treatment of some ROS- and age-related diseases (heart arrhythmia, heart infarctions, kidney ischemia, and stroke).

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Ultrastructure of the mitochondrion and its bearing on function and bioenergetics

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Mutant NDUFV2 subunit of mitochondrial complex I causes early onset hypertrophic cardiomyopathy and encephalopathy

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Large-scale deletion and point mutations of the nuclear NDUFV1 and NDUFS1 genes in mitochondrial complex I deficiency

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Mutant NDUFS3 subunit of mitochondrial complex I causes Leigh syndrome

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Mitochondrial complex I deficiency caused by a deleterious NDUFA11 mutation.

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A dynamic machinery for import of mitochondrial precursor proteins

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Mitochondrial dynamics--fusion, fission, movement, and mitophagy--in neurodegenerative diseases

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Resveratrol induces mitochondrial biogenesis in endothelial cells

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The antioxidant Trolox restores mitochondrial membrane potential and Ca2+ -stimulated ATP production in human complex I deficiency

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Human CIA30 is involved in the early assembly of mitochondrial complex I and mutations in its gene cause disease

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The architecture of respiratory complex I

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X-linked NDUFA1 gene mutations associated with mitochondrial encephalomyopathy.

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Mitochondria-targeted antioxidant SkQR1 selectively protects MDR (Pgp 170)-negative cells against oxidative stress

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Detection and manipulation of mitochondrial reactive oxygen species in mammalian cells

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Mitochondria-Targeted Antioxidant MitoQ 10 Improves Endothelial Function and Attenuates Cardiac Hypertrophy

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Sarco(endo)plasmic reticulum Ca2+ pump isoform SERCA3 is more resistant than SERCA2b to peroxide

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NDUFA2 complex I mutation leads to Leigh disease

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Some practical aspects of providing a diagnostic service for respiratory chain defects

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Mitochondrial complex I: structure, function and pathology

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Selective targeting of a redox-active ubiquinone to mitochondria within cells: antioxidant and antiapoptotic properties

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Mitigation of NADH: ubiquinone oxidoreductase deficiency by chronic Trolox treatment.

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Inhibition of complex I of the electron transport chain causes O2-. -mediated mitochondrial outgrowth.

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Inhibitors of the quinone-binding site allow rapid superoxide production from mitochondrial NADH:ubiquinone oxidoreductase (complex I).

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The first nuclear-encoded complex I mutation in a patient with Leigh syndrome

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Mutations in the complex I NDUFS2 gene of patients with cardiomyopathy and encephalomyopathy

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Grape extract protects mitochondria from oxidative damage and improves locomotor dysfunction and extends lifespan in a Drosophila Parkinson's disease model

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C6ORF66 is an assembly factor of mitochondrial complex I

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7 January 2021

Mutations in NDUFAF3 (C3ORF60), encoding an NDUFAF4 (C6ORF66)-interacting complex I assembly protein, cause fatal neonatal mitochondrial disease

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7 January 2021

Mutant NDUFV1 subunit of mitochondrial complex I causes leukodystrophy and myoclonic epilepsy.

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7 January 2021

Penetrating cation/fatty acid anion pair as a mitochondria-targeted protonophore.

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7 January 2021

Resveratrol protects mitochondria against oxidative stress through AMP-activated protein kinase-mediated glycogen synthase kinase-3beta inhibition downstream of poly(ADP-ribose)polymerase-LKB1 pathway

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7 January 2021

An attempt to prevent senescence: a mitochondrial approach.

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7 January 2021

The genetics and pathology of oxidative phosphorylation

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7 January 2021

Human NADH:ubiquinone oxidoreductase

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7 January 2021

Mutation of C20orf7 disrupts complex I assembly and causes lethal neonatal mitochondrial disease

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7 January 2021

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7 January 2021

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7 January 2021

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Resveratrol attenuates mitochondrial oxidative stress in coronary arterial endothelial cells

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7 January 2021

Demonstration of a new pathogenic mutation in human complex I deficiency: a 5-bp duplication in the nuclear gene encoding the 18-kD (AQDQ) subunit

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7 January 2021

Ca2+-mobilizing agonists increase mitochondrial ATP production to accelerate cytosolic Ca2+ removal: aberrations in human complex I deficiency.

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7 January 2021

Inhibition of mitochondrial Na+-Ca2+ exchange restores agonist-induced ATP production and Ca2+ handling in human complex I deficiency.

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7 January 2021

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7 January 2021

Mitochondrial Ca2+ homeostasis in human NADH:ubiquinone oxidoreductase deficiency.

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7 January 2021

Mechanism for resveratrol-induced cardioprotection against reperfusion injury involves glycogen synthase kinase 3beta and mitochondrial permeability transition pore.

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7 January 2021

Identifiers

DOI

10.1002/DDRR.107

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13 February 2020

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