The Role of Mitochondrial Redox Regulations in Inflammation and Disease

A special issue of Antioxidants (ISSN 2076-3921). This special issue belongs to the section "Health Outcomes of Antioxidants and Oxidative Stress".

Deadline for manuscript submissions: closed (31 July 2024) | Viewed by 1258

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Guest Editor
Department of Clinical and Movement Neurosciences, UCL Queen Square Institute of Neurology, University College London, London, UK
Interests: mitochondria; energy metabolism; neurodegeneration; Alzheimer’s disease; Parkinson’s disease; misfolded proteins; calcium homeostasis; calcium signaling; oxidative stress; ferroptosis; ROS signaling; epilepsy; ischemia; hypoxia; cancer; brain inorganic polyphosphate
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Special Issue Information

Dear Colleagues,

Redox-dependent processes regulate most of the cellular functions, such as proliferation, differentiation, and apoptosis. Mitochondria are cellular organelles with a pivotal role in many cellular processes, including the production and distribution of energy for all cellular functions, controlling the processes of quality control, protein transport, and biogenesis and programmed cell death, and the regulation of metabolic pathways, ionic homeostasis, thermogenesis, stress responses, cellular signaling, and inflammatory response. Mitochondria, on the one hand, generate reactive oxygen species (ROS) that drive redox-sensitive events and, on the other hand, respond to ROS-mediated changes in the cellular redox state. Therefore, any disruption of mitochondrial function is central to the development of a wide range of major human diseases.

This Special Issue is devoted to providing the latest insights into the role of mitochondrial redox regulation in the molecular mechanisms of mitochondrial redox signalling, the impact of mitochondrial dysfunction on cellular metabolism and inflammation, the role of mitochondrial redox regulation in the pathogenesis of various diseases such as cancer, cardiovascular disease and neurodegenerative disorders and the potential therapeutic implications of targeting mitochondrial redox signalling for the treatment of these diseases.

Dr. Plamena R. Angelova
Guest Editor

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Keywords

  • redox signalling
  • mitochondrial dysfunction
  • mitochondrial bioenergetics
  • mitochondrial dynamics
  • mitochondrial biogenesis
  • oxidative stress
  • inflammation
  • cancer
  • diabetes
  • neurodegeneration
  • cardiovascular diseases
  • ischemia-reperfusion injury

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Published Papers (1 paper)

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Review

11 pages, 1187 KiB  
Review
Carbon Monoxide: A Pleiotropic Redox Regulator of Life and Death
by Andrey Y. Abramov, Isabella Myers and Plamena R. Angelova
Antioxidants 2024, 13(9), 1121; https://doi.org/10.3390/antiox13091121 - 16 Sep 2024
Viewed by 803
Abstract
Despite recent technological progress, carbon monoxide poisoning is still one of the leading causes of domestic and industrial morbidity and mortality. The brain is particularly vulnerable to CO toxicity, and thus the majority of survivors develop delayed movement and cognitive complications. CO binds [...] Read more.
Despite recent technological progress, carbon monoxide poisoning is still one of the leading causes of domestic and industrial morbidity and mortality. The brain is particularly vulnerable to CO toxicity, and thus the majority of survivors develop delayed movement and cognitive complications. CO binds to haemoglobin in erythrocytes, preventing oxygen delivery to tissues, and additionally inhibits mitochondrial respiration. This renders the effect of CO to be closely related to hypoxia reperfusion injury. Oxygen deprivation, as well as CO poisoning and re-oxygenation, are shown to be able to activate the production of reactive oxygen species and to induce oxidative stress. Here, we review the role of reactive oxygen species production and oxidative stress in the mechanism of neuronal cell death induced by carbon monoxide and re-oxygenation. We discuss possible protective mechanisms used by brain cells with a specific focus on the inhibition of CO-induced ROS production and oxidative stress. Full article
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