{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,30]],"date-time":"2026-10-30T03:14:43Z","timestamp":1793330083381,"version":"4.5.0"},"reference-count":31,"publisher":"Wiley","license":[{"start":{"date-parts":[[2014,1,1]],"date-time":"2014-01-01T00:00:00Z","timestamp":1388534400000},"content-version":"unspecified","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/3.0\/"}],"funder":[{"DOI":"10.13039\/501100001868","name":"National Science Council","doi-asserted-by":"publisher","award":["NSC102-2314-B-002-023"],"award-info":[{"award-number":["NSC102-2314-B-002-023"]}],"id":[{"id":"10.13039\/501100001868","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Oxidative Medicine and Cellular Longevity"],"published-print":{"date-parts":[[2014]]},"abstract":"<jats:p>Human peritoneal mesothelial cells (HPMCs) are a critical component of the peritoneal membrane and play a pivotal role in dialysis adequacy. Loss of HPMCs can contribute to complications in peritoneal dialysis. Compelling evidence has shown that high-dialysate glucose is a key factor causing functional changes and cell death in HPMCs. We investigated the mechanism of HPMC apoptosis induced by high-dialysate glucose, particularly the role of mitochondria in the maintenance of HPMCs. HPMCs were incubated at glucose concentrations of 5\u2009mM, 84\u2009mM, 138\u2009mM, and 236\u2009mM. Additionally, N-acetylcysteine (NAC) was used as an antioxidant to clarify the mechanism of high-dialysate-glucose-induced apoptosis. Exposing HPMCs to high-dialysate glucose resulted in substantial apoptosis with cytochrome c release, followed by caspase activation and poly(ADP-ribose) polymerase cleavage. High-dialysate glucose induced excessive reactive oxygen species production and lipid peroxidation as well as oxidative damage to DNA. Mitochondrial fragmentation, multiple mitochondrial DNA deletions, and dissipation of the mitochondrial membrane potential were also observed. The mitochondrial dysfunction and cell death were suppressed using NAC. These results indicated that mitochondrial dysfunction is one of the main causes of high-dialysate-glucose-induced HPMC apoptosis.<\/jats:p>","DOI":"10.1155\/2014\/642793","type":"journal-article","created":{"date-parts":[[2014,5,5]],"date-time":"2014-05-05T21:15:53Z","timestamp":1399324553000},"page":"1-12","source":"Crossref","is-referenced-by-count":42,"title":["High-Dialysate-Glucose-Induced Oxidative Stress and Mitochondrial-Mediated Apoptosis in Human Peritoneal Mesothelial Cells"],"prefix":"10.1155","volume":"2014","author":[{"given":"Kuan-Yu","family":"Hung","sequence":"first","affiliation":[{"name":"Department of Internal Medicine, National Taiwan University Hospital, College of Medicine, National Taiwan University, Taipei 106, Taiwan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Shin-Yun","family":"Liu","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine, National Taiwan University Hospital, College of Medicine, National Taiwan University, Taipei 106, Taiwan"},{"name":"School of Medical Laboratory Science and Biotechnology, College of Medical Science and Technology, Taipei Medical University, Taipei 110, Taiwan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Te-Cheng","family":"Yang","sequence":"additional","affiliation":[{"name":"Division of Nephrology, Department of Internal Medicine, Kuan-Tien General Hospital, Taichung 433, Taiwan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Tien-Ling","family":"Liao","sequence":"additional","affiliation":[{"name":"School of Medical Laboratory Science and Biotechnology, College of Medical Science and Technology, Taipei Medical University, Taipei 110, Taiwan"},{"name":"Graduate Institute of Medical Science, College of Medicine, Taipei Medical University, Taipei 110, Taiwan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Shu-Huei","family":"Kao","sequence":"additional","affiliation":[{"name":"School of Medical Laboratory Science and Biotechnology, College of Medical Science and Technology, Taipei Medical University, Taipei 110, Taiwan"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"311","reference":[{"key":"1","doi-asserted-by":"publisher","DOI":"10.1038\/nrneph.2012.13"},{"issue":"3","key":"2","doi-asserted-by":"crossref","first-page":"334","DOI":"10.1016\/S0272-6386(97)90276-6","volume":"30","year":"1997","journal-title":"American Journal of Kidney Diseases"},{"issue":"88","key":"3","first-page":"S43","volume":"64","year":"2003","journal-title":"Kidney International"},{"key":"4","doi-asserted-by":"publisher","DOI":"10.1111\/j.1744-9987.2006.00391.x"},{"issue":"2","key":"5","doi-asserted-by":"crossref","first-page":"470","DOI":"10.1681\/ASN.V132470","volume":"13","year":"2002","journal-title":"Journal of the American Society of Nephrology"},{"key":"6","doi-asserted-by":"publisher","DOI":"10.1038\/labinvest.3700519"},{"key":"7","doi-asserted-by":"publisher","DOI":"10.1093\/ndt\/gfh277"},{"key":"8","doi-asserted-by":"publisher","DOI":"10.1111\/j.1523-1755.2005.00058.x"},{"key":"9","doi-asserted-by":"publisher","DOI":"10.1093\/ndt\/gfn369"},{"issue":"22","key":"10","first-page":"2922","volume":"15","year":"2001","journal-title":"Genes and Development"},{"key":"11","doi-asserted-by":"crossref","first-page":"99","DOI":"10.1042\/bse0470099","volume":"47","year":"2010","journal-title":"Essays in Biochemistry"},{"key":"12","doi-asserted-by":"publisher","DOI":"10.1002\/ajmg.1398"},{"issue":"1","key":"13","first-page":"S110","volume":"53","year":"2004","journal-title":"Diabetes"},{"issue":"3","key":"14","doi-asserted-by":"crossref","first-page":"F455","DOI":"10.1152\/ajprenal.00137.2002","volume":"284","year":"2003","journal-title":"American Journal of Physiology. 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