期刊
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
卷 509, 期 1, 页码 16-23出版社
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.bbrc.2018.11.137
关键词
Cardiac hypertrophy; LILRB4; Fibrosis; Inflammation and apoptosis; NF-kappa B
Pathological cardiac hypertrophy is a leading cause of morbidity and mortality in the world. However, it is still unclear the molecular mechanism revealing the progression of the disease. In the study, we illustrated that the expression of leukocyte immunoglobulin-like receptor B4 (LILRB4), associated with the pathological development of various inflammatory diseases, was down-regulated in pressure overload-induced hearts of patients and mice. LILRB4-knockout mice developed cardiac hypertrophy and heart failure by promoting cardiac dysfunction, fibrosis, inflammation and apoptosis. Mechanistically, transforming growth factor beta 1 (TGF-beta 1) expression was significantly promoted by LILRB4 deficiency in hearts of mice after aortic banding (AB) surgery. AB-induced inflammation in cardiac tissues was accelerated by LILRB4 deletion through elevating nuclear factor kappa B (NF-kappa B) signaling pathway. Furthermore, apoptosis triggered by AB operation in heart tissues was markedly enhanced in LILRB4-KO mice through promoting Caspase-3 activation. Importantly, the in vitro study indicated that LILRB4 knockdown-promoted fibrosis; inflammation and apoptosis were largely via the NF-kappa B signaling. Therefore, the findings above identified LILRB4 might be a negative regulator of cardiac remodeling, illustrating that LILRB4 represented as a therapeutic target for the prevention of cardiac hypertrophy and heart failure. (C) 2018 Published by Elsevier Inc.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据