Crosstalk between the heart and peripheral organs in heart failure.
Crosstalk between the heart and peripheral organs in heart failure.
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DOI：
10.1038/emm.2016.20
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发表时间：
2016-03-11
影响因子：
12.8
通讯作者：
Sweeney G
中科院分区：
文献类型：
--
作者：
Jahng JW;Song E;Sweeney G
外周组织中的介质可影响心力衰竭(HF)的发生和发展。例如，在肥胖中，脂肪组织分泌的脂肪因子的变化会增加心肌梗死(MI)的发生率。较少被认识到的是心脏重塑释放心脏因子，这可以强烈地影响各种外周组织。炎症，特别是核苷酸结合的寡聚化结构域样受体与吡咯结构域(NLRP3)炎症小体的激活，可能在心脏重构和与其他器官的串扰中发挥核心作用。心脏损伤后NLRP3型炎症小体的激活诱导炎性细胞因子IL-1、β和IL-18的产生和分泌。除了对心肌有局部作用外，这些促炎细胞因子还被释放到循环中，导致脾、肾、骨骼肌和脂肪组织的重塑。各种心脏因子对外周器官的共同作用取决于心肌损伤的程度和持续时间，随着心衰的进展，可观察到全身炎症和外周组织损伤。在本文中，我们综述了心衰时心肌炎症的调节机制以及心脏分泌的因子在与周围组织沟通中的作用。
Mediators from peripheral tissues can influence the development and progression of heart failure (HF). For example, in obesity, an altered profile of adipokines secreted from adipose tissue increases the incidence of myocardial infarction (MI). Less appreciated is that heart remodeling releases cardiokines, which can strongly impact various peripheral tissues. Inflammation, and, in particular, activation of the nucleotide-binding oligomerization domain-like receptors with pyrin domain (NLRP3) inflammasome are likely to have a central role in cardiac remodeling and mediating crosstalk with other organs. Activation of the NLRP3 inflammasome in response to cardiac injury induces the production and secretion of the inflammatory cytokines interleukin (IL)-1β and IL-18. In addition to having local effects in the myocardium, these pro-inflammatory cytokines are released into circulation and cause remodeling in the spleen, kidney, skeletal muscle and adipose tissue. The collective effects of various cardiokines on peripheral organs depend on the degree and duration of myocardial injury, with systematic inflammation and peripheral tissue damage observed as HF progresses. In this article, we review mechanisms regulating myocardial inflammation in HF and the role of factors secreted by the heart in communication with peripheral tissues.