https://scholars.lib.ntu.edu.tw/handle/123456789/522977
DC 欄位 | 值 | 語言 |
---|---|---|
dc.contributor.author | Chiu C.-Y. | en_US |
dc.contributor.author | RONG-SEN YANG | en_US |
dc.contributor.author | Sheu M.-L. | en_US |
dc.contributor.author | DING-CHENG CHAN | en_US |
dc.contributor.author | TING-HUA YANG | en_US |
dc.contributor.author | KEH-SUNG TSAI | en_US |
dc.contributor.author | CHIH-KANG CHIANG | en_US |
dc.contributor.author | Liu S.-H. | en_US |
dc.date.accessioned | 2020-11-30T06:15:18Z | - |
dc.date.available | 2020-11-30T06:15:18Z | - |
dc.date.issued | 2016 | - |
dc.identifier.issn | 0022-3417 | - |
dc.identifier.uri | https://www.scopus.com/inward/record.uri?eid=2-s2.0-84956585988&doi=10.1002%2fpath.4674&partnerID=40&md5=97ecea06c01f8c315cf8d6e4e997fb98 | - |
dc.identifier.uri | https://scholars.lib.ntu.edu.tw/handle/123456789/522977 | - |
dc.description.abstract | Diabetic myopathy, a less studied complication of diabetes, exhibits the clinical observations characterized by a less muscle mass, muscle weakness and a reduced physical functional capacity. Accumulation of advanced glycation end-products (AGEs), known to play a role in diabetic complications, has been identified in ageing human skeletal muscles. However, the role of AGEs in diabetic myopathy remains unclear. Here, we investigated the effects of AGEs on myogenic differentiation and muscle atrophy in vivo and in vitro. We also evaluated the therapeutic potential of alagebrium chloride (Ala-Cl), an inhibitor of AGEs. Muscle fibre atrophy and immunoreactivity for AGEs, Atrogin-1 (a muscle atrophy marker) and phosphorylated AMP-activated protein kinase (AMPK) expressions were markedly increased in human skeletal muscles from patients with diabetes as compared with control subjects. Moreover, in diabetic mice we found increased blood AGEs, less muscle mass, lower muscular endurance, atrophic muscle size and poor regenerative capacity, and increased levels of muscle AGE and receptor for AGE (RAGE), Atrogin-1 and phosphorylated AMPK, which could be significantly ameliorated by Ala-Cl. Furthermore, in vitro, AGEs (in a dose-dependent manner) reduced myotube diameters (myotube atrophy) and induced Atrogin-1 protein expression in myotubes differentiated from both mouse myoblasts and primary human skeletal muscle-derived progenitor cells. AGEs exerted a negative regulation of myogenesis of mouse and human myoblasts. Ala-Cl significantly inhibited the effects of AGEs on myotube atrophy and myogenesis. We further demonstrated that AGEs induced muscle atrophy/myogenesis impairment via a RAGE-mediated AMPK-down-regulation of the Akt signalling pathway. Our findings support that AGEs play an important role in diabetic myopathy, and that an inhibitor of AGEs may offer a therapeutic strategy for managing the dysfunction of muscle due to diabetes or ageing. ? 2015 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd. | en_US |
dc.publisher | John Wiley and Sons Ltd | en_US |
dc.relation.ispartof | Journal of Pathology | en_US |
dc.subject.classification | [SDGs]SDG3 | - |
dc.subject.other | 8 [4 (1 aminocyclobutyl)phenyl] 9 phenyl 1,2,4 triazolo[3,4 f][1,6]naphthyridin 3(2h) one; advanced glycation end product; advanced glycation end product receptor; alagebrium; atrogin 1; glycerol; hydroxymethylglutaryl coenzyme A reductase kinase; protein kinase B; advanced glycation end product; Fbxo32 protein, mouse; hydroxymethylglutaryl coenzyme A reductase kinase; mitogen activated protein kinase; MOK protein, human; muscle protein; thiazole derivative; tumor antigen; ubiquitin protein ligase; adult; aged; animal cell; animal experiment; animal model; Article; comparative study; controlled study; diabetes mellitus; down regulation; endurance; female; human; human cell; human tissue; immunoreactivity; in vitro study; in vivo study; male; mouse; muscle atrophy; muscle development; muscle exercise; muscle fatigue; muscle mass; muscle regeneration; muscle weakness; myoblast; myotube; nonhuman; priority journal; protein expression; protein phosphorylation; signal transduction; skeletal muscle; skeletal muscle atrophy; soleus muscle; very elderly; animal; atrophy; case control study; diabetes mellitus; Diabetes Mellitus, Experimental; metabolism; muscle weakness; Muscular Diseases; pathology; physiology; regeneration; skeletal muscle; skeletal muscle cell; Aged; AMP-Activated Protein Kinases; Animals; Antigens, Neoplasm; Atrophy; Case-Control Studies; Diabetes Mellitus; Diabetes Mellitus, Experimental; Down-Regulation; Glycosylation End Products, Advanced; Humans; Male; MAP Kinase Signaling System; Mice; Mitogen-Activated Protein Kinases; Muscle Fatigue; Muscle Fibers, Skeletal; Muscle Proteins; Muscle Weakness; Muscle, Skeletal; Muscular Diseases; Regeneration; Signal Transduction; SKP Cullin F-Box Protein Ligases; Thiazoles | - |
dc.title | Advanced glycation end-products induce skeletal muscle atrophy and dysfunction in diabetic mice via a RAGE-mediated, AMPK-down-regulated, Akt pathway | en_US |
dc.type | journal article | en |
dc.identifier.doi | 10.1002/path.4674 | - |
dc.identifier.pmid | 26586640 | - |
dc.identifier.scopus | 2-s2.0-84956585988 | - |
dc.relation.pages | 470-482 | en_US |
dc.relation.journalvolume | 238 | en_US |
dc.relation.journalissue | 3 | en_US |
item.cerifentitytype | Publications | - |
item.fulltext | no fulltext | - |
item.openairecristype | http://purl.org/coar/resource_type/c_6501 | - |
item.openairetype | journal article | - |
item.grantfulltext | none | - |
crisitem.author.dept | Orthopedic Surgery-NTUH | - |
crisitem.author.dept | Orthopedic Surgery | - |
crisitem.author.dept | Internal Medicine | - |
crisitem.author.dept | Geriatrics and Gerontology-NTUH | - |
crisitem.author.dept | Otolaryngology-NTUH | - |
crisitem.author.dept | Laboratory Medicine | - |
crisitem.author.dept | Laboratory Medicine-NTUH | - |
crisitem.author.dept | Toxicology | - |
crisitem.author.dept | Integrated Diagnostics and Therapeutics-NTUH | - |
crisitem.author.dept | Internal Medicine | - |
crisitem.author.dept | Internal Medicine-NTUH | - |
crisitem.author.dept | Institute of Food Safety and Health | - |
crisitem.author.dept | Center for Biotechnology | - |
crisitem.author.orcid | 0000-0002-0553-4779 | - |
crisitem.author.orcid | 0000-0003-2215-2243 | - |
crisitem.author.orcid | 0000-0002-7255-7065 | - |
crisitem.author.orcid | 0000-0001-8528-1566 | - |
crisitem.author.orcid | 0000-0001-9021-4616 | - |
crisitem.author.parentorg | National Taiwan University Hospital | - |
crisitem.author.parentorg | College of Medicine | - |
crisitem.author.parentorg | College of Medicine | - |
crisitem.author.parentorg | National Taiwan University Hospital | - |
crisitem.author.parentorg | National Taiwan University Hospital | - |
crisitem.author.parentorg | College of Medicine | - |
crisitem.author.parentorg | National Taiwan University Hospital | - |
crisitem.author.parentorg | College of Medicine | - |
crisitem.author.parentorg | National Taiwan University Hospital | - |
crisitem.author.parentorg | College of Medicine | - |
crisitem.author.parentorg | National Taiwan University Hospital | - |
crisitem.author.parentorg | College of Public Health | - |
crisitem.author.parentorg | Others: University-Level Research Centers | - |
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