PDF(Pubmed)
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.
摘要：
巨噬细胞调节炎症和组织修复过程。因此,需要更好地了解巨噬细胞在心力衰竭发病机制中的作用.在肥厚型心肌病患者中，NLRC5在循环单核细胞和心脏巨噬细胞中显著增加。NLRC5的髓系特异性缺失加重了压力超负荷引起的病理性心脏重塑和炎症。机械上,NLRC5与HSPA8相互作用并抑制巨噬细胞中的NF-κB通路。巨噬细胞中NLRC5的缺失促进了细胞因子如白细胞介素-6(IL-6)的分泌,影响心肌细胞肥大和心脏成纤维细胞活化。Tocilizumab,抗IL-6受体拮抗剂，可能是心脏重塑和慢性心力衰竭的一种新的治疗策略。
