ArticleStem cells (Dayton, Ohio)2012
Mitochondrial superoxide production negatively regulates neural progenitor proliferation and cerebral cortical development.
Article in Stem cells (Dayton, Ohio), 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 papers.
What it found
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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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
58 citing papers in PubMed, 88 citations in OpenAlex.
- The multifaceted role of ATM protein in neural stem/progenitor cell biology and neurogenesis: beyond DNA damage response.Frontiers in pharmacology · 2026Review
- Endogenous mitochondrial hydrogen peroxide regulates neurogenesis during cortical development.Redox biology · 2025Article
- Developmental stage-dependent transcriptomic responses to neonatal intraventricular hemorrhage.Journal of neuroinflammation · 2025Article
- Disruption of tryptophan metabolism by high-fat diet-triggered maternal immune activation promotes social behavioral deficits in male mice.Nature communications · 2025Article
- The Switching of the Type of a ROS Signal from Mitochondria: The Role of Respiratory Substrates and Permeability Transition.Antioxidants (Basel, Switzerland) · 2024Article
- Sulfide quinone oxidoreductase contributes to voltage sensing of the mitochondrial permeability transition pore.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2024Article
- Mitochondrial dysfunction in pancreatic acinar cells: mechanisms and therapeutic strategies in acute pancreatitis.Frontiers in immunology · 2024Review
- Identity, structure, and function of the mitochondrial permeability transition pore: controversies, consensus, recent advances, and future directions.Cell death and differentiation · 2023Review
- Emerging roles of mitochondria in animal regeneration.Cell regeneration (London, England) · 2023Review
- Deregulation of ER-mitochondria contact formation and mitochondrial calcium homeostasis mediated by VDAC in fragile X syndrome.Developmental cell · 2023Article
- Glutaminolysis and the Control of Neural Progenitors in Neocortical Development and Evolution.The Neuroscientist : a review journal bringing neurobiology, neurology and psychiatry · 2023Review
- Re-evaluation of the risks to public health related to the presence of bisphenol A (BPA) in foodstuffs.EFSA journal. European Food Safety Authority · 2023Article
- Mitochondrial Permeability Transition in Stem Cells, Development, and Disease.Advances in experimental medicine and biology · 2023Review
- Mitochondrial respiration and dynamics of in vivo neural stem cells.Development (Cambridge, England) · 2022Article
- Vitamin C Deficiency Reduces Neurogenesis and Proliferation in the SVZ and Lateral Ventricle Extensions of the Young Guinea Pig Brain.Antioxidants (Basel, Switzerland) · 2022Article
- Convergent Canonical Pathways in Autism Spectrum Disorder from Proteomic, Transcriptomic and DNA Methylation Data.International journal of molecular sciences · 2021Review
- Aging: All roads lead to mitochondria.Seminars in cell & developmental biology · 2021Article
- Molecular and cellular pathways contributing to brain aging.Behavioral and brain functions : BBF · 2021Review
- In Pursuit of Healthy Aging: Effects of Nutrition on Brain Function.International journal of molecular sciences · 2021Review
- Mitochondrial and Autophagic Regulation of Adult Neurogenesis in the Healthy and Diseased Brain.International journal of molecular sciences · 2021Review
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
Abstract
Although high amounts of reactive oxygen species (ROS) can damage cells, ROS can also play roles as second messengers, regulating diverse cellular processes. Here, we report that embryonic mouse cerebral cortical neural progenitor cells (NPCs) exhibit intermittent spontaneous bursts of mitochondrial superoxide (SO) generation (mitochondrial SO flashes) that require transient opening of membrane permeability transition pores (mPTP). This quantal SO production negatively regulates NPC self-renewal. Mitochondrial SO scavengers and mPTP inhibitors reduce SO flash frequency and enhance NPC proliferation, whereas prolonged mPTP opening and SO generation increase SO flash incidence and decrease NPC proliferation. The inhibition of NPC proliferation by mitochondrial SO involves suppression of extracellular signal-regulated kinases. Moreover, mice lacking SOD2 (SOD2-/- mice) exhibit significantly fewer proliferative NPCs and differentiated neurons in the embryonic cerebral cortex at midgestation compared with wild-type littermates. Cultured SOD2-/- NPCs exhibit a significant increase in SO flash frequency and reduced NPC proliferation. Taken together, our findings suggest that mitochondrial SO flashes negatively regulate NPC self-renewal in the developing cerebral cortex.
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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.