Pharmacological Modulators of Endoplasmic Reticulum Stress in Metabolic Diseases
DC Field | Value | Language |
---|---|---|
dc.contributor.author | Jung, Tae Woo | - |
dc.contributor.author | Choi, Kyung Mook | - |
dc.date.accessioned | 2021-09-04T03:24:08Z | - |
dc.date.available | 2021-09-04T03:24:08Z | - |
dc.date.created | 2021-06-18 | - |
dc.date.issued | 2016-02 | - |
dc.identifier.issn | 1661-6596 | - |
dc.identifier.uri | https://scholar.korea.ac.kr/handle/2021.sw.korea/89624 | - |
dc.description.abstract | The endoplasmic reticulum (ER) is the principal organelle responsible for correct protein folding, a step in protein synthesis that is critical for the functional conformation of proteins. ER stress is a primary feature of secretory cells and is involved in the pathogenesis of numerous human diseases, such as certain neurodegenerative and cardiometabolic disorders. The unfolded protein response (UPR) is a defense mechanism to attenuate ER stress and maintain the homeostasis of the organism. Two major degradation systems, including the proteasome and autophagy, are involved in this defense system. If ER stress overwhelms the capacity of the cell's defense mechanisms, apoptotic death may result. This review is focused on the various pharmacological modulators that can protect cells from damage induced by ER stress. The possible mechanisms for cytoprotection are also discussed. | - |
dc.language | English | - |
dc.language.iso | en | - |
dc.publisher | MDPI | - |
dc.subject | UNFOLDED PROTEIN RESPONSE | - |
dc.subject | PANCREATIC BETA-CELLS | - |
dc.subject | FATTY LIVER-DISEASE | - |
dc.subject | INDUCED INSULIN-RESISTANCE | - |
dc.subject | HUMAN CARDIAC-CELLS | - |
dc.subject | ER STRESS | - |
dc.subject | CHEMICAL CHAPERONES | - |
dc.subject | IN-VIVO | - |
dc.subject | INDUCED APOPTOSIS | - |
dc.subject | TRANSGENIC MICE | - |
dc.title | Pharmacological Modulators of Endoplasmic Reticulum Stress in Metabolic Diseases | - |
dc.type | Article | - |
dc.contributor.affiliatedAuthor | Choi, Kyung Mook | - |
dc.identifier.doi | 10.3390/ijms17020192 | - |
dc.identifier.scopusid | 2-s2.0-84956942711 | - |
dc.identifier.wosid | 000371830800029 | - |
dc.identifier.bibliographicCitation | INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES, v.17, no.2 | - |
dc.relation.isPartOf | INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES | - |
dc.citation.title | INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES | - |
dc.citation.volume | 17 | - |
dc.citation.number | 2 | - |
dc.type.rims | ART | - |
dc.type.docType | Review | - |
dc.description.journalClass | 1 | - |
dc.description.journalRegisteredClass | scie | - |
dc.description.journalRegisteredClass | scopus | - |
dc.relation.journalResearchArea | Biochemistry & Molecular Biology | - |
dc.relation.journalResearchArea | Chemistry | - |
dc.relation.journalWebOfScienceCategory | Biochemistry & Molecular Biology | - |
dc.relation.journalWebOfScienceCategory | Chemistry, Multidisciplinary | - |
dc.subject.keywordPlus | UNFOLDED PROTEIN RESPONSE | - |
dc.subject.keywordPlus | PANCREATIC BETA-CELLS | - |
dc.subject.keywordPlus | FATTY LIVER-DISEASE | - |
dc.subject.keywordPlus | INDUCED INSULIN-RESISTANCE | - |
dc.subject.keywordPlus | HUMAN CARDIAC-CELLS | - |
dc.subject.keywordPlus | ER STRESS | - |
dc.subject.keywordPlus | CHEMICAL CHAPERONES | - |
dc.subject.keywordPlus | IN-VIVO | - |
dc.subject.keywordPlus | INDUCED APOPTOSIS | - |
dc.subject.keywordPlus | TRANSGENIC MICE | - |
dc.subject.keywordAuthor | endoplasmic reticulum stress | - |
dc.subject.keywordAuthor | unfolded protein response | - |
dc.subject.keywordAuthor | AMPK-activated protein kinase | - |
dc.subject.keywordAuthor | glucagon-like peptide-1 | - |
dc.subject.keywordAuthor | peroxisome proliferator-activated receptors | - |
dc.subject.keywordAuthor | angiotensin II type 1 receptor blockers | - |
Items in ScholarWorks are protected by copyright, with all rights reserved, unless otherwise indicated.
(02841) 서울특별시 성북구 안암로 14502-3290-1114
COPYRIGHT © 2021 Korea University. All Rights Reserved.
Certain data included herein are derived from the © Web of Science of Clarivate Analytics. All rights reserved.
You may not copy or re-distribute this material in whole or in part without the prior written consent of Clarivate Analytics.