Effect of Cysteine on Methylglyoxal-Induced Renal Damage in Mesangial Cells
DC Field | Value | Language |
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dc.contributor.author | Lee, Jae Hyuk | - |
dc.contributor.author | Subedi, Lalita | - |
dc.contributor.author | Kim, Sun Yeou | - |
dc.date.available | 2020-04-06T06:40:11Z | - |
dc.date.created | 2020-04-02 | - |
dc.date.issued | 2020-01 | - |
dc.identifier.issn | 2073-4409 | - |
dc.identifier.uri | https://scholarworks.bwise.kr/gachon/handle/2020.sw.gachon/26178 | - |
dc.description.abstract | Methylglyoxal (MGO), a highly reactive dicarbonyl compound, is a key precursor of the formation of advanced glycation end products (AGEs). MGO and MGO-AGEs were reportedly increased in patients with diabetic dysfunction, including diabetic nephropathy. The activation of glyoxalase-I (GLO-I) increases MGO and MGO-AGE detoxification. MGO-mediated glucotoxicity can also be ameliorated by MGO scavengers such as N-acetylcysteine (NAC), aminoguanidine (AG), and metformin. In this study, we noted that l-cysteine demonstrated protective effects against MGO-induced glucotoxicity in renal mesangial cells. l-cysteine prevented MGO-induced apoptosis and necrosis, together with a reduction of reactive oxygen species (ROS) production in MES13 cells. Interestingly, l-cysteine significantly reduced MGO-AGE formation and also acted as an MGO-AGE crosslink breaker. Furthermore, l-cysteine treatment accelerated MGO catabolism to D-lactate via the upregulation of GLO-I. The reduction of AGE formation and induction of AGE breakdown, following l-cysteine treatment, further supports the potential use of l-cysteine as an alternative for the therapeutic control of MGO-induced renal complications in diabetes, especially against diabetic nephropathy. | - |
dc.language | 영어 | - |
dc.language.iso | en | - |
dc.publisher | MDPI | - |
dc.relation.isPartOf | CELLS | - |
dc.subject | GLYCATION END-PRODUCTS | - |
dc.subject | INDUCED APOPTOSIS | - |
dc.subject | N-ACETYLCYSTEINE | - |
dc.subject | INHIBITORS | - |
dc.subject | ACTIVATION | - |
dc.subject | CARNOSINE | - |
dc.subject | ARGININE | - |
dc.subject | RECEPTOR | - |
dc.subject | STRESS | - |
dc.title | Effect of Cysteine on Methylglyoxal-Induced Renal Damage in Mesangial Cells | - |
dc.type | Article | - |
dc.type.rims | ART | - |
dc.description.journalClass | 1 | - |
dc.identifier.wosid | 000515398200234 | - |
dc.identifier.doi | 10.3390/cells9010234 | - |
dc.identifier.bibliographicCitation | CELLS, v.9, no.1 | - |
dc.identifier.scopusid | 2-s2.0-85097732413 | - |
dc.citation.title | CELLS | - |
dc.citation.volume | 9 | - |
dc.citation.number | 1 | - |
dc.contributor.affiliatedAuthor | Lee, Jae Hyuk | - |
dc.contributor.affiliatedAuthor | Subedi, Lalita | - |
dc.contributor.affiliatedAuthor | Kim, Sun Yeou | - |
dc.type.docType | Article | - |
dc.subject.keywordAuthor | methylglyoxal | - |
dc.subject.keywordAuthor | advanced glycation end products | - |
dc.subject.keywordAuthor | l-cysteine | - |
dc.subject.keywordAuthor | glyoxalase-I | - |
dc.subject.keywordAuthor | diabetic nephropathy | - |
dc.subject.keywordPlus | GLYCATION END-PRODUCTS | - |
dc.subject.keywordPlus | INDUCED APOPTOSIS | - |
dc.subject.keywordPlus | N-ACETYLCYSTEINE | - |
dc.subject.keywordPlus | INHIBITORS | - |
dc.subject.keywordPlus | ACTIVATION | - |
dc.subject.keywordPlus | CARNOSINE | - |
dc.subject.keywordPlus | ARGININE | - |
dc.subject.keywordPlus | RECEPTOR | - |
dc.subject.keywordPlus | STRESS | - |
dc.relation.journalResearchArea | Cell Biology | - |
dc.relation.journalWebOfScienceCategory | Cell Biology | - |
dc.description.journalRegisteredClass | scie | - |
dc.description.journalRegisteredClass | scopus | - |
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