ArticlePloS one2011
Mitochondrial network determines intracellular ROS dynamics and sensitivity to oxidative stress through switching inter-mitochondrial messengers.
Article in PloS one, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 113 papers.
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Who cites it
113 citing papers in PubMed, 225 citations in OpenAlex.
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- Nonlinear Redox-Immune Coupling Under Low-Dose-Rate Radiation: A Compartment-Specific Framework for Biological Responses-A Narrative Review.Antioxidants (Basel, Switzerland) · 2026Review
- Endothelial mitochondrial homeostasis in the development and progression of atherosclerosis.Frontiers in cardiovascular medicine · 2026Review
- Mapping key mitochondrial genes in Alzheimer's disease through human tissue and iPSC derived neurons.Scientific reports · 2025Article
- Loss of Ezrin triggers mitochondrial dysfunction and oxidative stress, associated with neuronal cell death.Cell death discovery · 2025Article
- Three-dimensional human mucopolysaccharidosis IVA chondrocyte culture reveals significant impairments in the lysosomal-mitochondrial crosstalk.Scientific reports · 2025Article
- Role of macrophage ATP metabolism disorder in SiOPurinergic signalling · 2025Review
- Analysis of the Mitochondrial Dynamics in NAFLD: Drp1 as a Marker of Inflammation and Fibrosis.International journal of molecular sciences · 2025Article
- 457 nm LED blue light inhibits oral squamous cell carcinoma cell proliferation via the PI3K/AKT pathway and autophagy.Photochemical & photobiological sciences : Official journal of the European Photochemistry Association and the European Society for Photobiology · 2025Article
- Cellular and Transcriptional Responses of Human Bronchial Epithelial Cells to Delta-9-Tetrahydrocannabinol In Vitro.International journal of molecular sciences · 2025Article
- Porcine reproductive and respiratory syndrome virus nsp5 inhibits the activation of the Nrf2/HO-1 pathway by targeting p62 to antagonize its antiviral activity.Journal of virology · 2025Article
- Replicative Senescence in Mesenchymal Stem Cells: An In Vitro Study on Mitochondrial Dynamics and Metabolic Alterations.Antioxidants (Basel, Switzerland) · 2025Article
- Nuclear respiratory factor-1 (NRF1) induction as a powerful strategy to deter mitochondrial dysfunction and senescence in mesenchymal stem cells.Aging cell · 2025Article
- Nuclear respiratory factor-1 (NRF1) induction drives mitochondrial biogenesis and attenuates amyloid beta-induced mitochondrial dysfunction and neurotoxicity.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2025Article
- Mitochondria and myocardial ischemia/reperfusion injury: Effects of Chinese herbal medicine and the underlying mechanisms.Journal of pharmaceutical analysis · 2025Review
- Biochanin a modulates steroidogenesis and cellular metabolism in human granulosa cells through TAS2Rs activation: a spotlight on ovarian function.Reproductive biology and endocrinology : RB&E · 2025Article
- Adipose tissue dysfunction disrupts metabolic homeostasis: mechanisms linking fat dysregulation to disease.Frontiers in endocrinology · 2025Review
- MCU-i4, a mitochondrial CaOncology research · 2025Article
- Suppressing ROS Production of AIE Nanoprobes by Simple Matrices Optimization for CNS Cell Observation and Minimized Influence of Cytoskeleton Morphology.Chemical & biomedical imaging · 2024Article
53 more citing papers are in PubMed but not listed here.
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Oxidative stresses caused by reactive oxygen species (ROS) can induce rapid depolarization of inner mitochondrial membrane potential and subsequent impairment of oxidative phosphorylation. Damaged mitochondria produce more ROS, especially the superoxide anion (O(2)(-)) and hydrogen peroxide (H(2)O(2)), which potentiate mitochondria-driven ROS propagation, so-called ROS-induced ROS release (RIRR), via activation of an inter-mitochondria signaling network. Therefore, loss of function in only a fraction of mitochondria might eventually affect cell viability through this positive feedback loop. Since ROS are very short-lived molecules in the biological milieu, mitochondrial network dynamics, such as density, number, and spatial distribution, can affect mitochondria-driven ROS propagation. To address this issue, we developed a mathematical model using an agent-based modeling approach, and tested the effect of mitochondrial network dynamics on RIRR for mitochondria under various conditions. Simulation results show that the intracellular ROS signaling pattern, such as ROS propagation speed and oxidative stress vulnerability, are critically affected by mitochondrial network dynamics. Mitochondrial network dynamics of mitochondrial distribution, density, activity, and size can mediate inter-mitochondrial signaling under certain conditions and determine the identity of the ROS signaling pattern. We further elucidated the potential mechanism of these actions, i.e., conversion of major messenger molecules involved in ROS signaling. If the average distance between neighboring mitochondria is large or mitochondrial distribution becomes randomized, messenger molecule of the ROS signaling network can be switched from O(2)(-) to H(2)O(2). In this case, mitochondria-driven ROS propagation is efficiently blocked by introduction of excess cytosolic glutathione peroxidase 1, while introduction of cytosolic superoxide dismutase has no effect. Together, these results suggest that mitochondrial network dynamics is a major determinant for cellular responses to RIRR through changing the key messenger molecules.
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