ArticleThe Journal of biological chemistry2012
Glucose modulates respiratory complex I activity in response to acute mitochondrial dysfunction.
Article in The Journal of biological chemistry, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
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Who cites it
33 citing papers in PubMed, 59 citations in OpenAlex.
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- CDCP1/mitochondrial Src axis increases electron transport chain function to promote metastasis in triple-negative breast cancer.British journal of cancer · 2025Article
- Importance of De Novo Gene Evolution to Emerging Viral Threats: The ORF10 Strain-Restricted Orphan Gene of SARS-CoV-2 Promotes Pathogenesis.Molecular biology and evolution · 2025Article
- Impairment of Muscle Function Causes Pupal Lethality in Flies Expressing the Mitochondrial Alternative Oxidase.Biomolecules · 2025Article
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- Alternative oxidase causes cell type- and tissue-specific responses in mutator mice.Life science alliance · 2023Article
- Butyrate inhibits the mitochondrial complex Ι to mediate mitochondria-dependent apoptosis of cervical cancer cells.BMC complementary medicine and therapies · 2023Article
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- Spatial adjustment of bioenergetics, a possible determinant of contractile adaptation and development of contractile failure.Frontiers in molecular medicine · 2023Review
- Autophagy promotes cell survival by maintaining NAD levels.Developmental cell · 2022Article
- Tumor growth of neurofibromin-deficient cells is driven by decreased respiration and hampered by NADCell death and differentiation · 2022Article
- Mitochondrial complex I derived ROS regulate stress adaptation in Drosophila melanogaster.Redox biology · 2020Article
- Arabidopsis thaliana alternative dehydrogenases: a potential therapy for mitochondrial complex I deficiency? Perspectives and pitfalls.Orphanet journal of rare diseases · 2019Article
- Hyperoxia but not AOX expression mitigates pathological cardiac remodeling in a mouse model of inflammatory cardiomyopathy.Scientific reports · 2019Article
- Alternative oxidase confers nutritional limitation on Drosophila development.Journal of experimental zoology. Part A, Ecological and integrative physiology · 2019Article
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- Mitochondrial complex III is necessary for endothelial cell proliferation during angiogenesis.Nature metabolism · 2019Article
- CHCHD4 regulates tumour proliferation and EMT-related phenotypes, through respiratory chain-mediated metabolism.Cancer & metabolism · 2019Article
- Expression of the Alternative Oxidase Influences Jun N-Terminal Kinase Signaling and Cell Migration.Molecular and cellular biology · 2018Article
- Polyadenylation and degradation of structurally abnormal mitochondrial tRNAs in human cells.Nucleic acids research · 2018Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Proper coordination between glycolysis and respiration is essential, yet the regulatory mechanisms involved in sensing respiratory chain defects and modifying mitochondrial functions accordingly are unclear. To investigate the nature of this regulation, we introduced respiratory bypass enzymes into cultured human (HEK293T) cells and studied mitochondrial responses to respiratory chain inhibition. In the absence of respiratory chain inhibitors, the expression of alternative respiratory enzymes did not detectably alter cell physiology or mitochondrial function. However, in permeabilized cells NDI1 (alternative NADH dehydrogenase) bypassed complex I inhibition, whereas alternative oxidase (AOX) bypassed complex III or IV inhibition. In contrast, in intact cells the effects of the AOX bypass were suppressed by growth on glucose, whereas those produced by NDI1 were unaffected. Moreover, NDI1 abolished the glucose suppression of AOX-driven respiration, implicating complex I as the target of this regulation. Rapid Complex I down-regulation was partly released upon prolonged respiratory inhibition, suggesting that it provides an "emergency shutdown" system to regulate metabolism in response to dysfunctions of the oxidative phosphorylation. This system was independent of HIF1, mitochondrial superoxide, or ATP synthase regulation. Our findings reveal a novel pathway for adaptation to mitochondrial dysfunction and could provide new opportunities for combatting diseases.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.