巨噬细胞
心肌梗塞
医学
心功能曲线
脑源性神经营养因子
内科学
下调和上调
神经营养因子
心室重构
M2巨噬细胞
蛋白激酶B
神经营养素
心脏病学
环境富集
内分泌学
受体
心力衰竭
信号转导
生物
细胞生物学
体外
基因
生物化学
作者
Peiyuan Bai,Siqin Chen,Dai Jia,Li-hong Pan,Chaobao Liu,Jin Liu,Wei Li,Yang Yang,Mayu Sun,Naifu Wan,Wuwei Rong,Aijun Sun,Junbo Ge
出处
期刊:Science Advances
[American Association for the Advancement of Science (AAAS)]
日期:2022-04-29
卷期号:8 (17)
被引量:5
标识
DOI:10.1126/sciadv.abm3436
摘要
Macrophages play a vital role in cardiac repair following myocardial infarction (MI). An enriched environment (EE) is involved in the regulation of macrophage-related activities and disease progression; however, whether EE affects the phenotype and function of macrophages to improve postinfarction cardiac repair remains unknown. In this study, we found that EE improved cardiac function, decreased mortality, and ameliorated adverse ventricular remodeling in mice after MI, with these outcomes closely related to the increased survival of Ly6Clow macrophages and their CCR2-MHCIIlow subsets. EE increased the expression of brain-derived neurotrophic factor (BDNF) in the hypothalamus, leading to higher circulating levels of BDNF, which, in turn, regulated the cardiac macrophages. BDNF bound to tropomyosin receptor kinase B to activate downstream ERK1/2 and AKT pathways, promoting macrophage survival. These findings demonstrate that EE optimizes postinfarction cardiac repair and highlights the significance of EE as a previously unidentified strategy for impeding adverse ventricular remodeling.
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