Reactive Oxygen Species: Angels and Demons in the Life of a Neuron
Reactive oxygen species (ROS) have emerged as regulators of key processes supporting neuronal growth, function, and plasticity across lifespan. At normal physiological levels, ROS perform important roles as secondary messengers in diverse molecular processes such as regulating neuronal differentiati...
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Published in | NeuroSci Vol. 3; no. 1; pp. 130 - 145 |
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Main Authors | , , |
Format | Journal Article |
Language | English |
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01.03.2022
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ISSN | 2673-4087 2673-4087 |
DOI | 10.3390/neurosci3010011 |
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Abstract | Reactive oxygen species (ROS) have emerged as regulators of key processes supporting neuronal growth, function, and plasticity across lifespan. At normal physiological levels, ROS perform important roles as secondary messengers in diverse molecular processes such as regulating neuronal differentiation, polarization, synapse maturation, and neurotransmission. In contrast, high levels of ROS are toxic and can ultimately lead to cell death. Excitable cells, such as neurons, often require high levels of metabolic activity to perform their functions. As a consequence, these cells are more likely to produce high levels of ROS, potentially enhancing their susceptibility to oxidative damage. In addition, because neurons are generally post-mitotic, they may be subject to accumulating oxidative damage. Thus, maintaining tight control over ROS concentration in the nervous system is essential for proper neuronal development and function. We are developing a more complete understanding of the cellular and molecular mechanisms for control of ROS in these processes. This review focuses on ROS regulation of the developmental and functional properties of neurons, highlighting recent in vivo studies. We also discuss the current evidence linking oxidative damage to pathological conditions associated with neurodevelopmental and neurodegenerative disorders. |
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AbstractList | Reactive oxygen species (ROS) have emerged as regulators of key processes supporting neuronal growth, function, and plasticity across lifespan. At normal physiological levels, ROS perform important roles as secondary messengers in diverse molecular processes such as regulating neuronal differentiation, polarization, synapse maturation, and neurotransmission. In contrast, high levels of ROS are toxic and can ultimately lead to cell death. Excitable cells, such as neurons, often require high levels of metabolic activity to perform their functions. As a consequence, these cells are more likely to produce high levels of ROS, potentially enhancing their susceptibility to oxidative damage. In addition, because neurons are generally post-mitotic, they may be subject to accumulating oxidative damage. Thus, maintaining tight control over ROS concentration in the nervous system is essential for proper neuronal development and function. We are developing a more complete understanding of the cellular and molecular mechanisms for control of ROS in these processes. This review focuses on ROS regulation of the developmental and functional properties of neurons, highlighting recent in vivo studies. We also discuss the current evidence linking oxidative damage to pathological conditions associated with neurodevelopmental and neurodegenerative disorders. Reactive oxygen species (ROS) have emerged as regulators of key processes supporting neuronal growth, function, and plasticity across lifespan. At normal physiological levels, ROS perform important roles as secondary messengers in diverse molecular processes such as regulating neuronal differentiation, polarization, synapse maturation, and neurotransmission. In contrast, high levels of ROS are toxic and can ultimately lead to cell death. Excitable cells, such as neurons, often require high levels of metabolic activity to perform their functions. As a consequence, these cells are more likely to produce high levels of ROS, potentially enhancing their susceptibility to oxidative damage. In addition, because neurons are generally post-mitotic, they may be subject to accumulating oxidative damage. Thus, maintaining tight control over ROS concentration in the nervous system is essential for proper neuronal development and function. We are developing a more complete understanding of the cellular and molecular mechanisms for control of ROS in these processes. This review focuses on ROS regulation of the developmental and functional properties of neurons, highlighting recent in vivo studies. We also discuss the current evidence linking oxidative damage to pathological conditions associated with neurodevelopmental and neurodegenerative disorders.Reactive oxygen species (ROS) have emerged as regulators of key processes supporting neuronal growth, function, and plasticity across lifespan. At normal physiological levels, ROS perform important roles as secondary messengers in diverse molecular processes such as regulating neuronal differentiation, polarization, synapse maturation, and neurotransmission. In contrast, high levels of ROS are toxic and can ultimately lead to cell death. Excitable cells, such as neurons, often require high levels of metabolic activity to perform their functions. As a consequence, these cells are more likely to produce high levels of ROS, potentially enhancing their susceptibility to oxidative damage. In addition, because neurons are generally post-mitotic, they may be subject to accumulating oxidative damage. Thus, maintaining tight control over ROS concentration in the nervous system is essential for proper neuronal development and function. We are developing a more complete understanding of the cellular and molecular mechanisms for control of ROS in these processes. This review focuses on ROS regulation of the developmental and functional properties of neurons, highlighting recent in vivo studies. We also discuss the current evidence linking oxidative damage to pathological conditions associated with neurodevelopmental and neurodegenerative disorders. |
Author | Alexander, Kellianne Francis, Michael M. Biswas, Kasturi |
AuthorAffiliation | 2 Graduate Program in Neuroscience, Morningside Graduate School of Biomedical Sciences, UMass Chan Medical School, Worcester, MA 01605, USA 1 Department of Neurobiology, University of Massachusetts Chan Medical School, Worcester, MA 01605, USA; kasturi.biswas@umassmed.edu (K.B.); kellianne.alexander@umassmed.edu (K.A.) |
AuthorAffiliation_xml | – name: 1 Department of Neurobiology, University of Massachusetts Chan Medical School, Worcester, MA 01605, USA; kasturi.biswas@umassmed.edu (K.B.); kellianne.alexander@umassmed.edu (K.A.) – name: 2 Graduate Program in Neuroscience, Morningside Graduate School of Biomedical Sciences, UMass Chan Medical School, Worcester, MA 01605, USA |
Author_xml | – sequence: 1 givenname: Kasturi orcidid: 0000-0001-7243-1422 surname: Biswas fullname: Biswas, Kasturi – sequence: 2 givenname: Kellianne orcidid: 0000-0002-4572-2600 surname: Alexander fullname: Alexander, Kellianne – sequence: 3 givenname: Michael M. orcidid: 0000-0002-8076-6668 surname: Francis fullname: Francis, Michael M. |
BackLink | https://www.ncbi.nlm.nih.gov/pubmed/39484669$$D View this record in MEDLINE/PubMed |
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Keywords | C. elegans brain injury neurodegenerative disease synapse neurodevelopment oxidative stress |
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