Role of Autophagy in Endothelial Damage and Blood-Brain Barrier Disruption in Ischemic Stroke
DC Field | Value | Language |
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dc.contributor.author | Kim, Kyeong-A | - |
dc.contributor.author | Shin, Donggeun | - |
dc.contributor.author | Kim, Jeong-Hyeon | - |
dc.contributor.author | Shin, Young-Jun | - |
dc.contributor.author | Rajanikant, G. K. | - |
dc.contributor.author | Majid, Arshad | - |
dc.contributor.author | Baek, Seung-Hoon | - |
dc.contributor.author | Bae, Ok-Nam | - |
dc.date.accessioned | 2021-06-22T12:01:02Z | - |
dc.date.available | 2021-06-22T12:01:02Z | - |
dc.date.created | 2021-01-21 | - |
dc.date.issued | 2018-06 | - |
dc.identifier.issn | 0039-2499 | - |
dc.identifier.uri | https://scholarworks.bwise.kr/erica/handle/2021.sw.erica/6190 | - |
dc.description.abstract | The global burden of neurological diseases including stroke has significantly increased, 1 and an urgent need exists to develop new treatment strategies. Impairment of autophagic regulation has been observed in diseases including neurodegenerative diseases and ischemic stroke, suggesting that modulation of autophagy could be a potential therapeutic target. 2 Endothelial cells (ECs) maintain homeostasis by regulating the vascular tone and permeability and endothelial dysfunction is associated with diverse cardiovascular diseases (CVDs). The integrity of the blood-brain barrier (BBB), which shows selective permeability for substances into the brain, is significantly impaired under ischemic stroke. This review focuses on autophagy in endothelial dysfunction in the context of ischemic stroke and potential targets for therapeutic manipulation. | - |
dc.language | 영어 | - |
dc.language.iso | en | - |
dc.publisher | LIPPINCOTT WILLIAMS & WILKINS | - |
dc.title | Role of Autophagy in Endothelial Damage and Blood-Brain Barrier Disruption in Ischemic Stroke | - |
dc.type | Article | - |
dc.contributor.affiliatedAuthor | Bae, Ok-Nam | - |
dc.identifier.doi | 10.1161/STROKEAHA.117.017287 | - |
dc.identifier.scopusid | 2-s2.0-85053472657 | - |
dc.identifier.wosid | 000433388300051 | - |
dc.identifier.bibliographicCitation | STROKE, v.49, no.6, pp.1571 - 1579 | - |
dc.relation.isPartOf | STROKE | - |
dc.citation.title | STROKE | - |
dc.citation.volume | 49 | - |
dc.citation.number | 6 | - |
dc.citation.startPage | 1571 | - |
dc.citation.endPage | 1579 | - |
dc.type.rims | ART | - |
dc.type.docType | Article | - |
dc.description.journalClass | 1 | - |
dc.description.isOpenAccess | Y | - |
dc.description.journalRegisteredClass | scie | - |
dc.description.journalRegisteredClass | scopus | - |
dc.relation.journalResearchArea | Neurosciences & Neurology | - |
dc.relation.journalResearchArea | Cardiovascular System & Cardiology | - |
dc.relation.journalWebOfScienceCategory | Clinical Neurology | - |
dc.relation.journalWebOfScienceCategory | Peripheral Vascular Disease | - |
dc.subject.keywordPlus | FOCAL CEREBRAL-ISCHEMIA | - |
dc.subject.keywordPlus | PROGENITOR CELLS | - |
dc.subject.keywordPlus | OXIDATIVE STRESS | - |
dc.subject.keywordPlus | RAT MODEL | - |
dc.subject.keywordPlus | SELECTIVE AUTOPHAGY | - |
dc.subject.keywordPlus | PROTECTIVE ROLE | - |
dc.subject.keywordPlus | INJURY | - |
dc.subject.keywordPlus | NEUROPROTECTION | - |
dc.subject.keywordPlus | DYSFUNCTION | - |
dc.subject.keywordPlus | DEATH | - |
dc.subject.keywordAuthor | autophagy | - |
dc.subject.keywordAuthor | blood-brain barrier | - |
dc.subject.keywordAuthor | disease progression | - |
dc.subject.keywordAuthor | endothelial cells | - |
dc.subject.keywordAuthor | endothelial progenitor cells | - |
dc.identifier.url | https://www.ahajournals.org/doi/10.1161/STROKEAHA.117.017287 | - |
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