ArticleEndocrinology2012
Topiramate treatment protects blood-brain barrier pericytes from hyperglycemia-induced oxidative damage in diabetic mice.
Article in Endocrinology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 77 papers.
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Who cites it
77 citing papers in PubMed, 114 citations in OpenAlex.
- NSE, a potential biomarker, is closely connected to diabetic peripheral neuropathy.Diabetes care · 2013Trial
- Mitochondrial carbonic anhydrase-VB inhibition rescues brain endothelial stress and memory in Alzheimer's disease models.Science advances · 2026Article
- Hyperpolarized NMR study of the impact of alzheimer's disease on diabetes using a novel rat model.Journal of physiology and biochemistry · 2026Article
- Human brain pericytes protect the blood-brain barrier from triple-negative breast cancer cells while promoting tumor aggressiveness.Journal of cell communication and signaling · 2026Article
- Strategies for blood-brain barrier rejuvenation and repair.Nature reviews. Drug discovery · 2026Review
- Mitochondrial carbonic anhydrase-VB inhibition rescues brain endothelial stress and memory in Alzheimer's disease models.bioRxiv : the preprint server for biology · 2026Article
- A web-based radiomics nomogram combining MRI features and clinical data for predicting 30-day progression of acute ischemic stroke: a two-center study.Frontiers in neurology · 2026Article
- Blood-Brain Barrier Integrity and Transport of Major Hormones are Unchanged in Mice With Euglycemic Hyperinsulinemia.Endocrinology · 2025Article
- Novel Insights into the Mechanism and Treatment of Diabetes-Related Brain Complications: Focusing on the Blood-Brain Barrier Impairment.Aging and disease · 2025Review
- Pericytes and Diabetic Microangiopathies: Tissue Resident Mesenchymal Stem Cells with High Plasticity and Regenerative Capacity.International journal of molecular sciences · 2025Review
- Beta cells to brain cells: The pivotal role of insulin and glucose metabolism in Alzheimer's disease.Neuroprotection (Chichester, England) · 2025Review
- Carbonic anhydrase inhibitors prevent presymptomatic capillary flow disturbances in a model of cerebral amyloidosis.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025Article
- Should We Consider Neurodegeneration by Itself or in a Triangulation with Neuroinflammation and Demyelination? The Example of Multiple Sclerosis and Beyond.International journal of molecular sciences · 2024Review
- Hyperglycemia in a NOD Mice Model of Type-I Diabetes Aggravates Collagenase-Induced Intracerebral Hemorrhagic Injury.Biomedicines · 2024Article
- miR-378a-3p responds to physical activity by modulating insulin-mediated glucose uptake and tricarboxylic acid cycle in skeletal muscle.Genes & diseases · 2024Article
- Carbonic anhydrase, its inhibitors and vascular function.Frontiers in molecular biosciences · 2024Review
- Protective Effect of Topiramate against Diabetic Retinopathy and Computational Approach Recognizing the Role of NLRP3/IL-1β/TNF-α Signaling.Biomedicines · 2023Article
- Pericyte Loss in Diseases.Cells · 2023Review
- Cellular senescence and the blood-brain barrier: Implications for aging and age-related diseases.Experimental biology and medicine (Maywood, N.J.) · 2023Review
- The Effects of Viruses on Insulin Sensitivity and Blood-Brain Barrier Function.International journal of molecular sciences · 2023Review
17 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 3 institutions in 1 country.
Funding
Abstract
Diabetes mellitus causes cerebral microvasculature deterioration and cognitive decline. The specialized endothelial cells of cerebral microvasculature comprise the blood-brain barrier, and the pericytes (PC) that are in immediate contact with these endothelial cells are vital for blood-brain barrier integrity. In diabetes, increased mitochondrial oxidative stress is implicated as a mechanism for hyperglycemia-induced PC loss as a prerequisite leading to blood-brain barrier disruption. Mitochondrial carbonic anhydrases (CA) regulate the oxidative metabolism of glucose and thus play an important role in the generation of reactive oxygen species and oxidative stress. We hypothesize that the inhibition of mitochondrial CA would reduce mitochondrial oxidative stress, rescue cerebral PC loss caused by diabetes-induced oxidative stress, and preserve blood-brain barrier integrity. We studied the effects of pharmacological inhibition of mitochondrial CA activity on streptozotocin-diabetes-induced oxidative stress and PC loss in the mouse brain. At 3 wk of diabetes, there was significant oxidative stress; the levels of reduced glutathione were lower and those of 3-nitrotyrosine, 4-hydroxy-2-trans-nonenal, and superoxide dismutase were higher. Treatment of diabetic mice with topiramate, a potent mitochondrial CA inhibitor, prevented the oxidative stress caused by 3 wk of diabetes. A significant decline in cerebral PC numbers, at 12 wk of diabetes, was also rescued by topiramate treatment. These results provide the first evidence that inhibition of mitochondrial CA activity reduces diabetes-induced oxidative stress in the mouse brain and rescues cerebral PC dropout. Thus, mitochondrial CA may provide a new therapeutic target for oxidative stress related illnesses of the central nervous system.
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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.