ReviewAging and disease2016
Oxidation of K(+) Channels in Aging and Neurodegeneration.
Review in Aging and disease, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
25 citing papers in PubMed, 47 citations in OpenAlex.
- Effects of Voluntary Running Wheel Activity and Hypertension on the Brain of Female Spontaneously Hypertensive Rats (SHRs).International journal of molecular sciences · 2026Article
- Sympathetic motor neuron dysfunction is a missing link in age-associated sympathetic overactivity.eLife · 2024Article
- Sympathetic Motor Neuron Dysfunction is a Missing Link in Age-Associated Sympathetic Overactivity.bioRxiv : the preprint server for biology · 2024Article
- Progressive Excitability Changes in the Medial Entorhinal Cortex in the 3xTg Mouse Model of Alzheimer's Disease Pathology.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2023Article
- Article
- Identifying Aging and Alzheimer Disease-Associated Somatic Variations in Excitatory Neurons From the Human Frontal Cortex.Neurology. Genetics · 2023Article
- Article
- The brake matters: Hyperexcitable arousal circuits in sleep fragmentation with age.Clinical and translational medicine · 2022Article
- Spatial Distribution of Intracellular Ion Concentrations in Aggregate-Forming HeLa Cells Analyzed by μ-XRF Imaging.ChemistryOpen · 2022Article
- Hyperexcitable arousal circuits drive sleep instability during aging.Science (New York, N.Y.) · 2022Article
- Protein Kinase C Controls the Excitability of Cortical Pyramidal Neurons by Regulating Kv2.2 Channel Activity.Neuroscience bulletin · 2022Article
- Dopamine-Dependent QR2 Pathway Activation in CA1 Interneurons Enhances Novel Memory Formation.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2020Article
- Stat3 oxidation-dependent regulation of gene expression impacts on developmental processes and involves cooperation with Hif-1α.PloS one · 2020Article
- Ion channels as potential redox sensors in lysosomes.Channels (Austin, Tex.) · 2019Review
- RTA 408 Inhibits Interleukin-1β-Induced MMP-9 Expression via Suppressing Protein Kinase-Dependent NF-κB and AP-1 Activation in Rat Brain Astrocytes.International journal of molecular sciences · 2019Article
- Emerging Anti-Aging Strategies - Scientific Basis and Efficacy.Aging and disease · 2018Review
- Oxidation of KCNB1 channels in the human brain and in mouse model of Alzheimer's disease.Cell death & disease · 2018Article
- Redox Signaling in Neurotransmission and Cognition During Aging.Antioxidants & redox signaling · 2018Review
- Antioxidant properties of flavonoid derivatives and their hepatoprotective effects on CClRSC advances · 2018Article
- Herba Cistanches: Anti-aging.Aging and disease · 2017Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Reversible regulation of proteins by reactive oxygen species (ROS) is an important mechanism of neuronal plasticity. In particular, ROS have been shown to act as modulatory molecules of ion channels-which are key to neuronal excitability-in several physiological processes. However ROS are also fundamental contributors to aging vulnerability. When the level of excess ROS increases in the cell during aging, DNA is damaged, proteins are oxidized, lipids are degraded and more ROS are produced, all culminating in significant cell injury. From this arose the idea that oxidation of ion channels by ROS is one of the culprits for neuronal aging. Aging-dependent oxidative modification of voltage-gated potassium (K(+)) channels was initially demonstrated in the nematode Caenorhabditis elegans and more recently in the mammalian brain. Specifically, oxidation of the delayed rectifier KCNB1 (Kv2.1) and of Ca(2+)- and voltage sensitive K(+) channels have been established suggesting that their redox sensitivity contributes to altered excitability, progression of healthy aging and of neurodegenerative disease. Here I discuss the implications that oxidation of K(+) channels by ROS may have for normal aging, as well as for neurodegenerative disease.
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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.