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- W4317376761 abstract "Macrophages regulate inflammation and the process of tissue repair. Therefore, a better understanding of macrophages in the pathogenesis of heart failure is needed. In patients with hypertrophic cardiomyopathy, NLRC5 was significantly increased in circulating monocytes and cardiac macrophages. Myeloid-specific deletion of NLRC5 aggravated pressure overload-induced pathological cardiac remodeling and inflammation. Mechanistically, NLRC5 interacted with HSPA8 and suppressed NF-κB pathway in macrophages. The absence of NLRC5 in macrophages promoted the secretion of cytokines such as interleukin-6 (IL-6), which affected cardiomyocyte hypertrophy and cardiac fibroblast activation. Tocilizumab, an anti-IL-6 receptor antagonist, may be a novel therapeutic strategy for cardiac remodeling and chronic heart failure." @default.
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- W4317376761 date "2023-05-01" @default.
- W4317376761 modified "2023-09-26" @default.
- W4317376761 title "Macrophage-Specific NLRC5 Protects From Cardiac Remodeling Through Interaction With HSPA8" @default.
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- W4317376761 doi "https://doi.org/10.1016/j.jacbts.2022.10.001" @default.
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