ArticleNeural regeneration research2013
Control mechanisms in mitochondrial oxidative phosphorylation.
Article in Neural regeneration research, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers, 1 of them a synthesis that pooled it.
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Who cites it
44 citing papers in PubMed, 1 synthesis or guideline pooled it, 56 citations in OpenAlex.
- Mitochondrial enzyme dysfunction in Alzheimer's disease: a systematic review of human metabolic evidence.Metabolic brain disease · 2026Pooled it
- Wavelength dependent effects of red and infrared photobiomodulation on neuropathic pain, skeletal muscle integrity, and mitochondrial respiration.Lasers in medical science · 2026Article
- Bioinspired Artificial Bioenergetic Organelles: Design Principles, Nanofabrication and Therapeutic Translation.Advanced materials (Deerfield Beach, Fla.) · 2026Review
- Identification of the putative regulatory regions and candidate genes associated with backfat thickness and intramuscular fat content traits in Xiang pigs.BMC genomics · 2025Article
- Sulfide Quinone Oxidoreductase Alleviates Acute Ulcerative Colitis by Regulating Mitochondrial Dysfunction.MedComm · 2025Article
- Endocrine-disrupting effects of environmental BPS and PFOS on human brain organoid development.Frontiers in endocrinology · 2025Article
- Mitophagy Unveiled: Exploring the Nexus of Mitochondrial Health and Neuroendocrinopathy.Journal of molecular neuroscience : MN · 2024Review
- Leukocyte immunoglobulin-like receptor B1 (LILRB1) protects human multiple myeloma cells from ferroptosis by maintaining cholesterol homeostasis.Nature communications · 2024Article
- Mitochondrial Dysfunction of Astrocytes Mediates Lipid Accumulation in Temporal Lobe Epilepsy.Aging and disease · 2024Review
- CoQAntioxidants (Basel, Switzerland) · 2024Review
- Mitochondrial and Cellular Function in Fibroblasts, Induced Neurons, and Astrocytes Derived from Case Study Patients: Insights into Major Depression as a Mitochondria-Associated Disease.International journal of molecular sciences · 2024Article
- Oxidative phosphorylation in HIV-1 infection: impacts on cellular metabolism and immune function.Frontiers in immunology · 2024Review
- Article
- Effects of Deacetylase Inhibition on the Activation of the Antioxidant Response and Aerobic Metabolism in Cellular Models of Fanconi Anemia.Antioxidants (Basel, Switzerland) · 2023Article
- AnAzf1 acts as a positive regulator of ochratoxin A biosynthesis in Aspergillus niger.Applied microbiology and biotechnology · 2023Article
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- Dysregulation in Multiple Transcriptomic Endometrial Pathways Is Associated with Recurrent Implantation Failure and Recurrent Early Pregnancy Loss.International journal of molecular sciences · 2022Article
- Impairment of Mitochondrial Respiration in Metabolic Diseases: An Overview.International journal of molecular sciences · 2022Review
- Article
- Sodium dithionate (NaToxicology reports · 2022Article
Corrections and comments
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Authors and funding
2 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Distribution and activity of mitochondria are key factors in neuronal development, synaptic plasticity and axogenesis. The majority of energy sources, necessary for cellular functions, originate from oxidative phosphorylation located in the inner mitochondrial membrane. The adenosine-5'- triphosphate production is regulated by many control mechanism-firstly by oxygen, substrate level, adenosine-5'-diphosphate level, mitochondrial membrane potential, and rate of coupling and proton leak. Recently, these mechanisms have been implemented by "second control mechanisms," such as reversible phosphorylation of the tricarboxylic acid cycle enzymes and electron transport chain complexes, allosteric inhibition of cytochrome c oxidase, thyroid hormones, effects of fatty acids and uncoupling proteins. Impaired function of mitochondria is implicated in many diseases ranging from mitochondrial myopathies to bipolar disorder and schizophrenia. Mitochondrial dysfunctions are usually related to the ability of mitochondria to generate adenosine-5'-triphosphate in response to energy demands. Large amounts of reactive oxygen species are released by defective mitochondria, similarly, decline of antioxidative enzyme activities (e.g. in the elderly) enhances reactive oxygen species production. We reviewed data concerning neuroplasticity, physiology, and control of mitochondrial oxidative phosphorylation and reactive oxygen species production.
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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.