ArticleCommunicative & integrative biology2012
Contribution of mitochondrial network dynamics to intracellular ROS signaling.
Article in Communicative & integrative biology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 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.
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Who cites it
8 citing papers in PubMed, 18 citations in OpenAlex.
- Impact of chronic benzene poisoning on aberrant mitochondrial DNA methylation: A prospective observational study.Frontiers in public health · 2023Observational
- Mitochondrial Dynamin-Related Protein Drp1: a New Player in Cardio-oncology.Current oncology reports · 2022Review
- Mitochondrial Oxidative Phosphorylation defect in the Heart of Subjects with Coronary Artery Disease.Scientific reports · 2019Article
- Mitochondrial Fission Is Required for Blue Light-Induced Apoptosis and Mitophagy in Retinal Neuronal R28 Cells.Frontiers in molecular neuroscience · 2018Article
- Implication of Oxidative Stress in Fetal Programming of Cardiovascular Disease.Frontiers in physiology · 2018Review
- Metabolic Stress and Disorders Related to Alterations in Mitochondrial Fission or Fusion.Molecular and cellular pharmacology · 2013Article
- Mitochondrial signaling: forwards, backwards, and in between.Oxidative medicine and cellular longevity · 2013Review
- Exploring the electrostatic repulsion model in the role of Sirt3 in directing MnSOD acetylation status and enzymatic activity.Free radical biology & medicine · 2012Review
Corrections and comments
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Authors and funding
2 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Oxidative stresses can induce rapid depolarization of inner mitochondrial membrane potential and subsequent impairment of oxidative phosphorylation. Damaged mitochondria produce more reactive oxygen species (ROS), particularly the superoxide anion (O2-) 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-mitochondrial signaling network. In this context, mitochondrial network dynamics, such as their density, number, and spatial distribution, can affect mitochondria-driven ROS propagation. To investigate this inter-mitochondrial communication, 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 mitochondrial network dynamics are critical determinants of inter-mitochondrial ROS signaling patterns and main messenger ROS molecules. We further elucidated the potential mechanism of these actions, which is conversion of major messenger molecules involved in ROS signaling. Collectively, we propose that mitochondrial network dynamics can determine cellular responses to oxidative stress by switching the molecular species involved in cellular signaling.
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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.