NOX4-derived ROS are neuroprotective by balancing intracellular calcium stores

Hyperexcitability is associated with neuronal dysfunction, cellular death, and consequently neurodegeneration. Redox disbalance can contribute to hyperexcitation and increased reactive oxygen species (ROS) levels are observed in various neurological diseases. NOX4 is an NADPH oxidase known to produc...

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Published in:Cellular and molecular life sciences : CMLS 2023-05, Vol.80 (5), p.127-127, Article 127
Main Authors: Gola, Lukas, Bierhansl, Laura, Csatári, Júlia, Schroeter, Christina B., Korn, Lisanne, Narayanan, Venu, Cerina, Manuela, Abdolahi, Sara, Speicher, Anna, Hermann, Alexander M., König, Simone, Dinkova-Kostova, Albena T., Shekh-Ahmad, Tawfeeq, Meuth, Sven G., Wiendl, Heinz, Gorji, Ali, Pawlowski, Matthias, Kovac, Stjepana
Format: Article
Language:English
Subjects:
Alzheimer's disease
Apoptosis
Biochemistry
Bioenergetics
Biomedical and Life Sciences
Biomedicine
Brain diseases
Brain research
Calcium
Calcium (intracellular)
Calcium (mitochondrial)
Calcium homeostasis
Cell Biology
Cell death
Cells
Enzymes
Epilepsy
Function analysis
Homeostasis
Humans
Ischemia
Life Sciences
Localization
Metabolism
Mitochondria
NAD(P)H oxidase
NADPH Oxidase 4
NADPH Oxidases - metabolism
Neural networks
Neurodegeneration
Neurological diseases
Neurology
Neuroprotection
NOX4 protein
Original
Original Article
Oxidative Stress
Proteomics
Reactive Oxygen Species
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Summary:Hyperexcitability is associated with neuronal dysfunction, cellular death, and consequently neurodegeneration. Redox disbalance can contribute to hyperexcitation and increased reactive oxygen species (ROS) levels are observed in various neurological diseases. NOX4 is an NADPH oxidase known to produce ROS and might have a regulating function during oxidative stress. We, therefore, aimed to determine the role of NOX4 on neuronal firing, hyperexcitability, and hyperexcitability-induced changes in neural network function. Using a multidimensional approach of an in vivo model of hyperexcitability, proteomic analysis, and cellular function analysis of ROS, mitochondrial integrity, and calcium levels, we demonstrate that NOX4 is neuroprotective by regulating ROS and calcium homeostasis and thereby preventing hyperexcitability and consequently neuronal death. These results implicate NOX4 as a potential redox regulator that is beneficial in hyperexcitability and thereby might have an important role in neurodegeneration.
ISSN:1420-682X
1420-9071
DOI:10.1007/s00018-023-04758-z