Role of β-cell autophagy in β-cell physiology and the development of diabetes
DC Field | Value | Language |
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dc.contributor.author | Yasasilka, Xaviera Riani | - |
dc.contributor.author | Lee, Myung-Shik | - |
dc.date.accessioned | 2024-06-11T08:30:25Z | - |
dc.date.available | 2024-06-11T08:30:25Z | - |
dc.date.issued | 2024-06 | - |
dc.identifier.issn | 2040-1116 | - |
dc.identifier.issn | 2040-1124 | - |
dc.identifier.uri | https://scholarworks.bwise.kr/sch/handle/2021.sw.sch/26219 | - |
dc.description.abstract | Elucidating the molecular mechanism of autophagy was a landmark in understanding not only the physiology of cells and tissues, but also the pathogenesis of diverse diseases, including diabetes and metabolic disorders. Autophagy of pancreatic beta-cells plays a pivotal role in the maintenance of the mass, structure and function of beta-cells, whose dysregulation can lead to abnormal metabolic profiles or diabetes. Modulators of autophagy are being developed to improve metabolic profile and beta-cell function through the removal of harmful materials and rejuvenation of organelles, such as mitochondria and endoplasmic reticulum. Among the known antidiabetic drugs, glucagon-like peptide-1 receptor agonists enhance the autophagic activity of beta-cells, which might contribute to the profound effects of glucagon-like peptide-1 receptor agonists on systemic metabolism. In this review, the results from studies on the role of autophagy in beta-cells and their implication in the development of diabetes are discussed. In addition to non-selective (macro)autophagy, the role and mechanisms of selective autophagy and other minor forms of autophagy that might occur in beta-cells are discussed. As beta-cell failure is the ultimate cause of diabetes and unresponsiveness to conventional therapy, modulation of beta-cell autophagy might represent a future antidiabetic treatment approach, particularly in patients who are not well managed with current antidiabetic therapy. | - |
dc.format.extent | 13 | - |
dc.language | 영어 | - |
dc.language.iso | ENG | - |
dc.publisher | WILEY | - |
dc.title | Role of β-cell autophagy in β-cell physiology and the development of diabetes | - |
dc.type | Article | - |
dc.publisher.location | 미국 | - |
dc.identifier.doi | 10.1111/jdi.14184 | - |
dc.identifier.scopusid | 2-s2.0-85187479581 | - |
dc.identifier.wosid | 001182512000001 | - |
dc.identifier.bibliographicCitation | JOURNAL OF DIABETES INVESTIGATION, v.15, no.6, pp 656 - 668 | - |
dc.citation.title | JOURNAL OF DIABETES INVESTIGATION | - |
dc.citation.volume | 15 | - |
dc.citation.number | 6 | - |
dc.citation.startPage | 656 | - |
dc.citation.endPage | 668 | - |
dc.type.docType | Review | - |
dc.description.isOpenAccess | Y | - |
dc.description.journalRegisteredClass | scie | - |
dc.description.journalRegisteredClass | scopus | - |
dc.relation.journalResearchArea | Endocrinology & Metabolism | - |
dc.relation.journalWebOfScienceCategory | Endocrinology & Metabolism | - |
dc.subject.keywordPlus | ISLET AMYLOID POLYPEPTIDE | - |
dc.subject.keywordPlus | ENDOPLASMIC-RETICULUM TURNOVER | - |
dc.subject.keywordPlus | GLUCAGON-LIKE PEPTIDE-1 | - |
dc.subject.keywordPlus | DISTINCT PATHWAYS | - |
dc.subject.keywordPlus | ADAPTIVE RESPONSE | - |
dc.subject.keywordPlus | STRESS | - |
dc.subject.keywordPlus | INSULIN | - |
dc.subject.keywordPlus | AMPK | - |
dc.subject.keywordPlus | MITOPHAGY | - |
dc.subject.keywordPlus | CLEC16A | - |
dc.subject.keywordAuthor | beta-Cells | - |
dc.subject.keywordAuthor | Autophagy | - |
dc.subject.keywordAuthor | Lysosome | - |
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