ArticleFrontiers in physiology2021
Altered Jagged1-Notch1 Signaling in Enhanced Dysfunctional Neovascularization and Delayed Angiogenesis After Ischemic Stroke in HFD/STZ Induced Type 2 Diabetes Rats.
Article in Frontiers in physiology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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7 citing papers in PubMed, 9 citations in OpenAlex.
- Review
- Dexmedetomidine Promotes Angiogenesis After Ischemic Stroke Through the NRF2/HO-1/VEGF Pathway.Neurochemical research · 2025Article
- Semaglutide restores astrocyte-vascular interactions and blood-brain barrier integrity in a model of diet-induced metabolic syndrome.Diabetology & metabolic syndrome · 2025Article
- Exercise rescues cognitive impairment through inhibiting the fibrinogen neuroinflammative pathway in diabetes.Metabolic brain disease · 2024Article
- Exploring Chinese herbal medicine for ischemic stroke: insights into microglia and signaling pathways.Frontiers in pharmacology · 2024Review
- Polydatin attenuates tubulointerstitial fibrosis in diabetic kidney disease by inhibiting YAP expression and nuclear translocation.Frontiers in physiology · 2022Article
- Bailing capsule (Frontiers in pharmacology · 2022Article
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9 authors at 7 institutions in 1 country.
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Abstract
Diabetes exacerbates brain damage in cerebral ischemic stroke. Our previous study has demonstrated that after cerebral ischemia, type 2 diabetes rats displayed worse neurological outcomes, larger cerebral infarction and severer blood-brain barrier disruption. However, our knowledge of the mechanisms of how diabetes impacts the cerebrovascular repair process is limited. This study was aimed to characterize structural alterations and potential mechanisms in brain microvessels before and after ischemic stroke in type 2 diabetic rats treated with high-fat diet and streptozotocin (HFD/STZ). Furtherly, we tested our hypothesis that dysregulated intercellular Jagged1-Notch1 signaling was involved in the dysfunctional cerebral neovascularization both before and after ischemic stroke in HFD/STZ rats. In our study, we found increased yet dysfunctional neovascularization with activated Jagged1-Notch1 signaling in the cerebrovasculature before cerebral ischemia in HFD/STZ rats compared with non-diabetic rats. Furthermore, we observed delayed angiogenesis as well as suppressed Jagged1-Notch1 signaling after ischemic stroke. Our results elucidate the potential mechanisms underlying diabetes-related cerebral microvasculature dysfunction after ischemic stroke.
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