ArticleThe Journal of pharmacology and experimental therapeutics2013
Pharmacological inhibition of mitochondrial carbonic anhydrases protects mouse cerebral pericytes from high glucose-induced oxidative stress and apoptosis.
Article in The Journal of pharmacology and experimental therapeutics, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.
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Who cites it
41 citing papers in PubMed, 57 citations in OpenAlex.
- Mitochondrial carbonic anhydrase-VB inhibition rescues brain endothelial stress and memory in Alzheimer's disease models.Science advances · 2026Article
- Mitochondrial carbonic anhydrase-VB inhibition rescues brain endothelial stress and memory in Alzheimer's disease models.bioRxiv : the preprint server for biology · 2026Article
- Diabetes associated pericyte metabolic signatures and pathogenesis of diabetic retinopathy.Frontiers in endocrinology · 2026Review
- Metabolic reprogramming and interventions in angiogenesis.Journal of advanced research · 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
- Structure based exploration of mitochondrial alpha carbonic anhydrase inhibitors as potential leads for anti-obesity drug development.Daru : journal of Faculty of Pharmacy, Tehran University of Medical Sciences · 2024Review
- Pericyte loss initiates microvascular dysfunction in the development of diastolic dysfunction.European heart journal open · 2024Article
- FDA-approved carbonic anhydrase inhibitors reduce amyloid β pathology and improve cognition, by ameliorating cerebrovascular health and glial fitness.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2023Article
- Pericyte Loss in Diseases.Cells · 2023Review
- The Sub-Molecular and Atomic Theory of Cancer Beginning: The Role of Mitochondria.Diagnostics (Basel, Switzerland) · 2022Article
- Molecular mechanisms of coronary microvascular endothelial dysfunction in diabetes mellitus: focus on mitochondrial quality surveillance.Angiogenesis · 2022Review
- Inhibitors of Mitochondrial Human Carbonic Anhydrases VA and VB as a Therapeutic Strategy against Paclitaxel-Induced Neuropathic Pain in Mice.International journal of molecular sciences · 2022Article
- The Mighty Mitochondria Are Unifying Organelles and Metabolic Hubs in Multiple Organs of Obesity, Insulin Resistance, Metabolic Syndrome, and Type 2 Diabetes: An Observational Ultrastructure Study.International journal of molecular sciences · 2022Review
- Endothelial AMPKα1/PRKAA1 exacerbates inflammation in HFD-fed mice.British journal of pharmacology · 2022Article
- Clinical relevance of glucose metrics during the early brain injury period after aneurysmal subarachnoid hemorrhage: An opportunity for continuous glucose monitoring.Frontiers in neurology · 2022Review
- The Blood-Brain Barrier, Oxidative Stress, and Insulin Resistance.Antioxidants (Basel, Switzerland) · 2021Review
- Molecular processes mediating hyperhomocysteinemia-induced metabolic reprogramming, redox regulation and growth inhibition in endothelial cells.Redox biology · 2021Article
- Oxidative Stress and the Neurovascular Unit.Life (Basel, Switzerland) · 2021Review
- Celastrol Prevents Oxidative Stress Effects on FSHR, PAPP, and CYP19A1 Gene Expression in Cultured Human Granulosa-Lutein Cells.International journal of molecular sciences · 2021Article
- Pericytes: Intrinsic Transportation Engineers of the CNS Microcirculation.Frontiers in physiology · 2021Review
Corrections and comments
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Authors and funding
9 authors at 5 institutions in 2 countries.
Funding
Abstract
Diabetes-associated complications in the microvasculature of the brain are caused by oxidative stress, generated by overproduction of reactive oxygen species from hyperglycemia-induced accelerated oxidative metabolism of glucose. Pericytes, essential for the viability of the microvasculature, are especially susceptible to oxidative stress. Mitochondrial carbonic anhydrases, regulators of the oxidative metabolism of glucose, determine the rate of reactive oxygen species production and inhibition of mitochondrial carbonic anhydrases rescues glucose-induced pericyte loss in the diabetic mouse brain. We hypothesized that high glucose induces intracellular oxidative stress and pericyte apoptosis and that inhibition of mitochondrial carbonic anhydrases protects pericytes from oxidative stress-induced apoptosis. To validate our hypothesis, conditionally immortalized cerebral pericyte (IPC) cultures were established from Immortomice to investigate the effect of high glucose on oxidative stress and pericyte apoptosis. The IPCs expressed pericyte markers and induced high transendothelial electrical resistance and low permeability in brain endothelial cell monolayers comparable with pericytes in primary cultures. The IPCs also secreted cytokines constitutively and in response to lipopolysaccharide similar to pericytes. High glucose caused oxidative stress and apoptosis of these cells, with both oxidative stress and apoptosis significantly reduced after mitochondrial carbonic anhydrase inhibition. These results provide the first evidence that pharmacological inhibition of mitochondrial carbonic anhydrases attenuates pericyte apoptosis caused by high glucose-induced oxidative stress. Carbonic anhydrase inhibitors have a long history of safe clinical use and can be immediately evaluated for this new indication in translational research. Thus, mitochondrial carbonic anhydrases may provide a new therapeutic target for oxidative stress-related illnesses of the brain.
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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.