| http://purl.uniprot.org/citations/32692720 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/32692720 | http://www.w3.org/2000/01/rdf-schema#comment | "In this study, we investigated the role of macrophage stimulating 1 (Mst1) and the AMPK-Sirt1 signaling pathway in the oxidative stress-induced mitochondrial dysfunction and apoptosis seen in rheumatoid arthritis-related fibroblast-like synoviocytes (RA-FLSs). Mst1 mRNA and protein expression was significantly higher in hydrogen peroxide (H2O2)-treated RA-FLSs than untreated controls. H2O2 treatment induced the mitochondrial apoptotic pathway by activating caspase3/9 and Bax in the RA-FLSs. Moreover, H2O2 treatment significantly reduced mitochondrial membrane potential and mitochondrial state-3 and state-4 respiration, but increased reactive oxygen species (ROS). Mst1 silencing significantly reduced oxidative stress-induced mitochondrial dysfunction and apoptosis in RA-FLSs. Sirt1 expression was significantly reduced in the H2O2-treated RA-FLSs, but was higher in the H2O2-treated Mst1-silenced RA-FLSs. Pretreatment with selisistat (Sirt1-specific inhibitor) or compound C (AMPK antagonist) significantly reduced the viability and mitochondrial function in H2O2-treated Mst1-silenced RA-FLSs by inhibiting Sirt1 function or Sirt1 expression, respectively. These findings demonstrate that oxidative stress-related upregulation and activation of Mst1 promotes mitochondrial dysfunction and apoptosis in RA-FLSs by inhibiting the AMPK-Sirt1 signaling pathway. This suggests the Mst1-AMPK-Sirt1 axis is a potential target for RA therapy."xsd:string |
| http://purl.uniprot.org/citations/32692720 | http://purl.org/dc/terms/identifier | "doi:10.18632/aging.103643"xsd:string |
| http://purl.uniprot.org/citations/32692720 | http://purl.uniprot.org/core/author | "Wang Y."xsd:string |
| http://purl.uniprot.org/citations/32692720 | http://purl.uniprot.org/core/author | "Yang Q."xsd:string |
| http://purl.uniprot.org/citations/32692720 | http://purl.uniprot.org/core/author | "Shen S."xsd:string |
| http://purl.uniprot.org/citations/32692720 | http://purl.uniprot.org/core/author | "Zhang L."xsd:string |
| http://purl.uniprot.org/citations/32692720 | http://purl.uniprot.org/core/author | "Xiang Y."xsd:string |
| http://purl.uniprot.org/citations/32692720 | http://purl.uniprot.org/core/author | "Weng X."xsd:string |
| http://purl.uniprot.org/citations/32692720 | http://purl.uniprot.org/core/date | "2020"xsd:gYear |
| http://purl.uniprot.org/citations/32692720 | http://purl.uniprot.org/core/name | "Aging (Albany NY)"xsd:string |
| http://purl.uniprot.org/citations/32692720 | http://purl.uniprot.org/core/pages | "16211-16223"xsd:string |
| http://purl.uniprot.org/citations/32692720 | http://purl.uniprot.org/core/title | "Mst1 promotes mitochondrial dysfunction and apoptosis in oxidative stress-induced rheumatoid arthritis synoviocytes."xsd:string |
| http://purl.uniprot.org/citations/32692720 | http://purl.uniprot.org/core/volume | "12"xsd:string |
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