ReviewFrontiers in molecular biosciences2016
Dynamics of Human Mitochondrial Complex I Assembly: Implications for Neurodegenerative Diseases.
Review in Frontiers in molecular biosciences, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 73 papers, 2 of them syntheses that pooled it.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
73 citing papers in PubMed, 2 syntheses or guidelines pooled it, 118 citations in OpenAlex.
- A systematic review on the biochemical threshold of mitochondrial genetic variants.Genome research · 2024Pooled it
- Multivariate meta-analyses of mitochondrial complex I and IV in major depressive disorder, bipolar disorder, schizophrenia, Alzheimer disease, and Parkinson disease.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2019Pooled it
- Mitochondrial complex I as a master regulator of redox signaling: From structural architecture to directionality of electron transport.Free radical biology & medicine · 2026Review
- Article
- Mitochondrial complex I in focus: mechanisms and therapeutic strategies of urinary system diseases.Frontiers in physiology · 2026Review
- Disturbances in Mitochondrial Network, Biogenesis, and Mitochondria-Mediated Inflammatory Responses in Selected Brain Structures of Rats Exposed to Lead (Pb) During Prenatal and Neonatal Development.International journal of molecular sciences · 2025Article
- Comprehensive and In-Depth Molecular and Pathway Studies of the Hippocampus in Alzheimer's Disease.Cellular and molecular neurobiology · 2025Article
- Novel differentially expressed genes and multiple biological pathways for Alzheimer's disease identified in brain tissue from African American donors.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025Article
- Homocysteine interferes with Ndufa1 leading to mitochondrial dysfunction through repression of the NADCell death & disease · 2025Article
- Hidden β-γ Dehydrogenation Products in Long-Chain Fatty Acid Oxidation Unveiled by NMR: Implications on Lipid Metabolism.ACS bio & med chem Au · 2025Article
- High frequency of mitochondrial DNA rearrangements in the peripheral blood of adults with intellectual disability.Journal of intellectual disability research : JIDR · 2025Article
- Gene expression comparisons between captive and wild shrew brains reveal captivity effects.Biology letters · 2025Article
- Chronological Dynamics of Neuroinflammatory Responses in a High-Fat Diet Mouse Model.International journal of molecular sciences · 2024Article
- Article
- Exploring Intrinsic Disorder in Human Synucleins and Associated Proteins.International journal of molecular sciences · 2024Article
- Alternative splicing expands the clinical spectrum of NDUFS6-related mitochondrial disorders.Genetics in medicine : official journal of the American College of Medical Genetics · 2024Article
- Review
- DecipheringmSystems · 2024Article
- A novel inhibitor of the mitochondrial respiratory complex I with uncoupling properties exerts potent antitumor activity.Cell death & disease · 2024Article
- CLPP-Null Eukaryotes with Excess Heme Biosynthesis Show Reduced L-arginine Levels, Probably via CLPX-Mediated OAT Activation.Biomolecules · 2024Article
13 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Neurons are extremely energy demanding cells and highly dependent on the mitochondrial oxidative phosphorylation (OXPHOS) system. Mitochondria generate the energetic potential via the respiratory complexes I to IV, which constitute the electron transport chain (ETC), together with complex V. These redox reactions release energy in the form of ATP and also generate reactive oxygen species (ROS) that are involved in cell signaling but can eventually lead to oxidative stress. Complex I (CI or NADH:ubiquinone oxidoreductase) is the largest ETC enzyme, containing 44 subunits and the main contributor to ROS production. In recent years, the structure of the CI has become available and has provided new insights into CI assembly. A number of chaperones have been identified in the assembly and stability of the mature holo-CI, although they are not part of its final structure. Interestingly, CI dysfunction is the most common OXPHOS disorder in humans and defects in the CI assembly process are often observed. However, the dynamics of the events leading to CI biogenesis remain elusive, which precludes our understanding of how ETC malfunctioning affects neuronal integrity. Here, we review the current knowledge of the structural features of CI and its assembly factors and the potential role of CI misassembly in human disorders such as Complex I Deficiencies or Alzheimer's and Parkinson's 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.