ArticleDiabetes2015
Diabetic Stroke Severity: Epigenetic Remodeling and Neuronal, Glial, and Vascular Dysfunction.
Article in Diabetes, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
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Who cites it
33 citing papers in PubMed, 44 citations in OpenAlex.
- Deciphering the disease ecosystem of ischemic stroke via multi-omics and prospects for therapeutic strategies.Frontiers in neuroscience · 2026Review
- Bradykinin Type 2 Receptor Deficiency Reshapes Acute Neuroinflammation and Improves Cell Survival after Ischemic Stroke in Diabetic Mice.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2025Article
- Type 2 Diabetes Mellitus Exacerbates Brain Injury AfterBrain sciences · 2025Article
- Stress hyperglycemia ratio as a biomarker for early mortality risk stratification in cardiovascular disease: a propensity-matched analysis.Cardiovascular diabetology · 2025Observational
- Pathophysiological Mechanisms of Diabetes-Induced Macrovascular and Microvascular Complications: The Role of Oxidative Stress.Medical sciences (Basel, Switzerland) · 2025Review
- Assessment of stress hyperglycemia ratio to predict all-cause mortality in patients with critical cerebrovascular disease: a retrospective cohort study from the MIMIC-IV database.Cardiovascular diabetology · 2025Article
- Potential therapeutic targets for ischemic stroke in pre-clinical studies: Epigenetic-modifying enzymes DNMT/TET and HAT/HDAC.Frontiers in pharmacology · 2025Review
- Targeting oxidative stress in diabetic retinopathy: mechanisms, pathology, and novel treatment approaches.Frontiers in immunology · 2025Review
- Ischemic Stroke and the Biological Hallmarks of Aging.Aging and disease · 2024Review
- Article
- Effect and Mechanism of Sodium Butyrate on Neuronal Recovery and Prognosis in Diabetic Stroke.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2023Article
- Epigenetic mechanisms and potential therapeutic targets in stroke.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2022Review
- Ibrutinib ameliorates cerebral ischemia/reperfusion injury through autophagy activation and PI3K/Akt/mTOR signaling pathway in diabetic mice.Bioengineered · 2021Article
- Article
- Understanding the Connection Between Common Stroke Comorbidities, Their Associated Inflammation, and the Course of the Cerebral Ischemia/Reperfusion Cascade.Frontiers in immunology · 2021Review
- Oxidative stress and diabetic retinopathy: Molecular mechanisms, pathogenetic role and therapeutic implications.Redox biology · 2020Review
- Analysis of potential hub genes involved in the pathogenesis of Chinese type 1 diabetic patients.Annals of translational medicine · 2020Article
- Article
- A high methionine, low folate and vitamin BNeural regeneration research · 2019Article
- Inhibition of HDAC3 Ameliorates Cerebral Ischemia Reperfusion Injury in Diabetic Mice In Vivo and In Vitro.Journal of diabetes research · 2019Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
We determined the mechanism of severity during type 1 diabetic (T1D) stroke (ischemia-reperfusion [IR] injury) that affects potential markers associated with epigenetics, neuronal, glial, and vascular components of the brain with regard to nondiabetic stroke. The study used male genetic T1D Ins2(+/-) Akita and wild-type (C57BL/6J) mice. The experimental mice groups were 1) sham, 2) IR, 3) sham(Akita), and 4) IR(Akita). Mice were subjected to middle cerebral artery occlusion for 40 min, followed by reperfusion for 24 h. Brain tissues were analyzed for inflammation, neuro-glio-vascular impairments, matrix metalloproteinase (MMP)-9 expression, and epigenetic alterations (DNA methyltransferase-3a [DNMT-3a]; DNA methyltransferase-1 [DNMT-1]; 5-methylcytosine [5-mC]; and 5-hydroxymethylcytosine [5-hmC]). Intracarotid fluorescein isothiocyanate-BSA infusion was used to determine pial-venular permeability. IR(Akita) mice showed more infarct volume, edema, inflammation, and vascular MMP-9 expression compared with IR and sham groups. Sham(Akita) mice showed the highest DNMT-1 and DNMT-3a levels compared with the other groups. Reduced tight and adherent junction expressions and severe venular leakage exemplified intense cerebrovascular impairment in IR(Akita) mice compared with the other groups. Interestingly, we found differential regulations (downregulated expression) of epigenetic (5-mC, DNMTs), vascular (endothelial nitric oxide synthase), glial (connexin-43, glial fibrillary acidic protein, CD11b), and neuronal (neuron-specific enolase, neuronal nitric oxide synthase) markers in IR(Akita) compared with the IR group. These findings suggest that IR injury in T1D is more severe because it intensifies differential epigenetic markers and neuro-glio-vascular changes compared with nondiabetic mice.
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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.