ArticleFree radical biology & medicine2018
Altered mitochondrial acetylation profiles in a kainic acid model of temporal lobe epilepsy.
Article in Free radical biology & medicine, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 50 citations in OpenAlex.
- Crotonylation of STXBP1 exacerbates seizure susceptibility by impairing GABAergic synaptic transmission.Cell death and differentiation · 2026Article
- Metabolic Alterations Induced by a Seizure-Causing Sodium Channel Mutation and their Partial Normalization by Dietary α-Linolenic Acid in Drosophila.Neurochemical research · 2026Article
- Mitochondrial dysfunction and NLRP3 inflammasome activation in drug-resistant epilepsy: emerging insights and mitochondrial-targeted therapeutic strategies.Naunyn-Schmiedeberg's archives of pharmacology · 2025Review
- Beyond Impaired GABAergic Signaling: Inflammation and Metabolic Dysfunction in Genetic Epilepsy Induced by GABRG2 Mutation.Molecular neurobiology · 2025Article
- Mitochondrial dysfunction in epilepsy: mechanistic insights and clinical strategies.Molecular biology reports · 2025Review
- Anti-epileptic and Neuroprotective Effects of Ultra-low Dose NADPH Oxidase Inhibitor Dextromethorphan on Kainic Acid-induced Chronic Temporal Lobe Epilepsy in Rats.Neuroscience bulletin · 2024Article
- A Compared Study of Eicosapentaenoic Acid and Docosahexaenoic Acid in Improving Seizure-Induced Cognitive Deficiency in a Pentylenetetrazol-Kindling Young Mice Model.Marine drugs · 2023Article
- Neuronal SIRT3 Deletion Predisposes to Female-Specific Alterations in Cellular Metabolism, Memory, and Network Excitability.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2023Article
- Role of SIRT3 in neurological diseases and rehabilitation training.Metabolic brain disease · 2023Review
- HAT- and HDAC-Targeted Protein Acetylation in the Occurrence and Treatment of Epilepsy.Biomedicines · 2022Review
- The Brain Protein Acylation System Responds to Seizures in the Rat Model of PTZ-Induced Epilepsy.International journal of molecular sciences · 2022Article
- Cytochrome P450-mediated antiseizure medication interactions influence apoptosis, modulate the brain BAX/Bcl-XFrontiers in pharmacology · 2022Article
- Progress on mitochondrial silence information regulator family in epilepsy.Zhejiang da xue xue bao. Yi xue ban = Journal of Zhejiang University. Medical sciences · 2021Review
- Asiatic Acid Prevents Cognitive Deficits by Inhibiting Calpain Activation and Preserving Synaptic and Mitochondrial Function in Rats with Kainic Acid-Induced Seizure.Biomedicines · 2021Article
- Acetylation Profiles in the Metabolic Process of Glioma-Associated Seizures.Frontiers in neurology · 2021Article
- Pathological Targets for Treating Temporal Lobe Epilepsy: Discoveries From Microscale to Macroscale.Frontiers in neurology · 2021Review
- A unifying mechanism of ketogenic diet action: The multiple roles of nicotinamide adenine dinucleotide.Epilepsy research · 2020Review
- Inhibition of miR-181a-5p reduces astrocyte and microglia activation and oxidative stress by activating SIRT1 in immature rats with epilepsy.Laboratory investigation; a journal of technical methods and pathology · 2020Article
- Antioxidants Targeting Mitochondrial Oxidative Stress: Promising Neuroprotectants for Epilepsy.Oxidative medicine and cellular longevity · 2020Review
- Neuroproteomics in Epilepsy: What Do We Know so Far?Frontiers in molecular neuroscience · 2020Review
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
Abstract
Impaired bioenergetics and oxidative damage in the mitochondria are implicated in the etiology of temporal lobe epilepsy, and hyperacetylation of mitochondrial proteins has recently emerged as a critical negative regulator of mitochondrial functions. However, the roles of mitochondrial acetylation and activity of the primary mitochondrial deacetylase, SIRT3, have not been explored in acquired epilepsy. We investigated changes in mitochondrial acetylation and SIRT3 activity in the development of chronic epilepsy in the kainic acid rat model of TLE. Hippocampal measurements were made at 48 h, 1 week and 12 weeks corresponding to the acute, latent and chronic stages of epileptogenesis. Assessment of hippocampal bioenergetics demonstrated a ≥ 27% decrease in the ATP/ADP ratio at all phases of epileptogenesis (p < 0.05), whereas cellular NAD+ levels were decreased by ≥ 41% in the acute and latent time points (p < 0.05), but not in chronically epileptic rats. In spontaneously epileptic rats, we found decreased protein expression of SIRT3 and a 60% increase in global mitochondrial acetylation, as well as enhanced acetylation of the known SIRT3 substrates MnSOD, Ndufa9 of Complex I and IDH2 (all p < 0.05), suggesting SIRT3 dysfunction in chronic epilepsy. Mass spectrometry-based acetylomics investigation of hippocampal mitochondria demonstrated a 79% increase in unique acetylated proteins from rats in the chronic phase vs. controls. Pathway analysis identified numerous mitochondrial bioenergetic pathways affected by mitochondrial acetylation. These results suggest SIRT3 dysfunction and aberrant protein acetylation may contribute to mitochondrial dysfunction in chronic epilepsy.
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