The Role of Endoplasmic Reticulum Stress in Cardiovascular Disease and Exercise
DC Field | Value | Language |
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dc.contributor.author | Hong, Junyoung | - |
dc.contributor.author | Kim, Kwangchan | - |
dc.contributor.author | Kim, Jong-Hee | - |
dc.contributor.author | Park, Yoonjung | - |
dc.date.accessioned | 2022-07-14T23:37:41Z | - |
dc.date.available | 2022-07-14T23:37:41Z | - |
dc.date.created | 2021-05-12 | - |
dc.date.issued | 2017 | - |
dc.identifier.issn | 2090-2824 | - |
dc.identifier.uri | https://scholarworks.bwise.kr/hanyang/handle/2021.sw.hanyang/153242 | - |
dc.description.abstract | Endoplasmic reticulum (ER) stress, which is highly associated with cardiovascular disease, is triggered by a disturbance in ER function because of protein misfolding or an increase in protein secretion. Prolonged disruption of ER causes ER stress and activation of the unfolded protein response (UPR) and leads to various diseases. Eukaryotic cells respond to ER stress via three major sensors that are bound to the ER membrane: activating transcription factor 6 (ATF6), inositol-requiring protein 1 alpha (IRE1 alpha), and protein kinase RNA-like ER kinase (PERK). Chronic activation of ER stress causes damage in endothelial cells (EC) via apoptosis, inflammation, and oxidative stress signaling pathways. The alleviation of ER stress has recently been accepted as a potential therapeutic target to treat cardiovascular diseases such as heart failure, hypertension, and atherosclerosis. Exercise training is an effective nonpharmacological approach for preventing and alleviating cardiovascular disease. We here review the recent viewing of ER stress-mediated apoptosis and inflammation signaling pathways in cardiovascular disease and the role of exercise in ER stress-associated diseases. | - |
dc.language | 영어 | - |
dc.language.iso | en | - |
dc.publisher | HINDAWI LTD | - |
dc.title | The Role of Endoplasmic Reticulum Stress in Cardiovascular Disease and Exercise | - |
dc.type | Article | - |
dc.contributor.affiliatedAuthor | Kim, Jong-Hee | - |
dc.identifier.doi | 10.1155/2017/2049217 | - |
dc.identifier.scopusid | 2-s2.0-85028329122 | - |
dc.identifier.wosid | 000407922700001 | - |
dc.identifier.bibliographicCitation | INTERNATIONAL JOURNAL OF VASCULAR MEDICINE, v.2017, pp.1 - 10 | - |
dc.relation.isPartOf | INTERNATIONAL JOURNAL OF VASCULAR MEDICINE | - |
dc.citation.title | INTERNATIONAL JOURNAL OF VASCULAR MEDICINE | - |
dc.citation.volume | 2017 | - |
dc.citation.startPage | 1 | - |
dc.citation.endPage | 10 | - |
dc.type.rims | ART | - |
dc.type.docType | Review | - |
dc.description.journalClass | 1 | - |
dc.description.isOpenAccess | Y | - |
dc.description.journalRegisteredClass | scopus | - |
dc.relation.journalResearchArea | Cardiovascular System & Cardiology | - |
dc.relation.journalWebOfScienceCategory | Peripheral Vascular Disease | - |
dc.subject.keywordPlus | UNFOLDED PROTEIN RESPONSE | - |
dc.subject.keywordPlus | NF-KAPPA-B | - |
dc.subject.keywordPlus | NECROSIS-FACTOR-ALPHA | - |
dc.subject.keywordPlus | THIOREDOXIN-INTERACTING PROTEIN | - |
dc.subject.keywordPlus | CORONARY-ARTERY FUNCTION | - |
dc.subject.keywordPlus | NEURONAL CELL-DEATH | - |
dc.subject.keywordPlus | INDUCED ER STRESS | - |
dc.subject.keywordPlus | TNF-ALPHA | - |
dc.subject.keywordPlus | ENDOTHELIAL DYSFUNCTION | - |
dc.subject.keywordPlus | SKELETAL-MUSCLE | - |
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