Crosstalk between the heart and peripheral organs in heart failure

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.

Relationship between Heart Disease and Liver Disease: A Two-Way Street

“…It consists of a multi-protein signaling platform that acts as an intracellular innate immune sensor and its activation induces the transcription, maturation, and release of proinflammatory cytokines, in particular IL-1β and IL-18. In heart failure, three main triggers contribute to the activation of NLRP3 inflammasome components: adenosine triphosphate (ATP), mitochondrial DNA (mtDNA), and reactive oxygen species (ROS) [122]. Despite the clear evidence that cardiokinesare involved in the crosstalk between myocardial inflammation in heart failure and peripheral tissue damage in some organs (adipose, tissue, skeletal muscle, spleen, and kidney), direct mechanisms linking heart and liver disease remain not fully characterized.…”

The neutrophil to lymphocyte ratio in heart failure: a comprehensive review

“…The initial cytokine hypothesis postulated that endogenous cytokines induce HF progression [3]. However, more and more data support the reverse theory as well, proving that HF induces inflammation in both the myocardium itself as well as other tissues and organs [4]. Regardless of the HF substrate, its multiple possible etiologies or its coinciding risk factors, inflammation parameters are related to HF prognosis, with worst outcomes in patients with more prevalent and higher expression of inflammatory biomarkers [5].…”

The Prognostic Impact of Circulating Regulatory T Lymphocytes on Mortality in Patients with Ischemic Heart Failure with Reduced Ejection Fraction

“…Recently, proinflammatory cytokines proved to have a pivotal role in the development and progression of HFrEF-however, less attention has been paid to the impact of cellular immunity. Shear stress and inflammatory mediators released by damaged myocardial tissue encourage sterile inflammation among myocytes and subsequently cardiac fibrosis [14] in HFrEF. Besides affecting the cardiac tissue itself, released cytokines proved to indirectly impact other organs as well [14,15].…”