%0 Journal Article
%T Macrophage-Specific NLRC5 Protects From Cardiac Remodeling Through Interaction With HSPA8.
%A Yu Q
%A Ju P
%A Kou W
%A Zhai M
%A Zeng Y
%A Maimaitiaili N
%A Shi Y
%A Xu X
%A Zhao Y
%A Jian W
%A Feinberg MW
%A Xu Y
%A Zhuang J
%A Peng W
%J JACC Basic Transl Sci
%V 8
%N 5
%D 2023 May
%M 37325412
%F 9.531
%R 10.1016/j.jacbts.2022.10.001
%X 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.