Exp Mol Med.  2016 Mar;48(3):e217. 10.1038/emm.2016.20.

Crosstalk between the heart and peripheral organs in heart failure

• Jahng JW
• Song E
• Sweeney G

• KMID: 2361504
• DOI: http://doi.org/10.1038/emm.2016.20

Abstract

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.

MeSH Terms

Adipokines
Adipose Tissue
Cytokines
Heart Failure*
Heart*
Incidence
Inflammasomes
Inflammation
Interleukin-18
Interleukins
Kidney
Muscle, Skeletal
Myocardial Infarction
Myocardium
Negotiating
Obesity
Spleen
Adipokines
Cytokines
Inflammasomes
Interleukin-18
Interleukins