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• W2897238384 abstract "Rheumatoid arthritis (RA) is a chronic inflammatory disorder characterized by destructive polyarthritis and systemic complications. It increases cardiovascular morbidity and mortality. However, the mechanism underlying RA-related cardiac damage remains largely unknown. Here, we found and characterized a non-human primate (NHP) model with spontaneous RA similar to the human conditions. Compared with the control group, the cardiac function in RA monkeys showed progressively deterioration; histologically, we found significantly increased inflammatory cell infiltration, cell death, and fibrosis in RA monkey heart tissue. Mechanistically, the upregulated receptor-interacting protein kinase 1 (RIPK1) in RA monkey heart tissue bound to voltage-dependent anion-selective channel 1 (VDAC1), increased VDAC1 oligomerization, and subsequently induced cardiac cell death and functional impairment. These findings identified that RIPK1-VDAC1 pathway is a promising target to treat cardiac impairment in RA. This unique model of RA will provide a valuable tool for mechanistic and translational studies." @default.
• W2897238384 created "2018-10-26" @default.
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• W2897238384 date "2018-12-01" @default.
• W2897238384 modified "2023-10-15" @default.
• W2897238384 title "Central role of RIPK1-VDAC1 pathway on cardiac impairment in a non-human primate model of rheumatoid arthritis" @default.
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• W2897238384 doi "https://doi.org/10.1016/j.yjmcc.2018.10.015" @default.
• W2897238384 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/30339841" @default.
• W2897238384 hasPublicationYear "2018" @default.
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