Table 1 Cytokines/chemokines involved in crosstalk between the heart and peripheral organs
From: Crosstalk between the heart and peripheral organs in heart failure
Cytokines/Chemokines | Effect | Reference |
---|---|---|
Neutrophil activation and leukocyte infiltration | ||
[@Spleen] increasing mobility and inflammatory characteristics of monocytes, and infiltration of DCs to heart | ||
[@Heart] autocrine production of IL-6, TNFα | ||
Prolonged exposure led to pyroptosis | ||
Pro-inflammatory cytokines | ||
DAMPs, HMGB1, DNA fragments, heat shock proteins, matricellular protein9, 55, 56, 57 | [@Heart] autocrine effects to produce pro-inflammatory cytokines; IL-1β, IL-18, IL-6, MCP-1, TNFα | |
Prolonged exposure led to pyroptosis | ||
[@Skeletal Muscle] muscle wasting, sphingosine production, induction of apoptosis | ||
ANP71 | Paracrine effect: oxytocin production, reducing lipid peroxidation with NO-dependent mechanism | |
[@Heart] autocrine effect on heart by increasing expression of contractile protein, actin and myosin, and induce hypertrophy | ||
[@Adipose Tissue] enhancing lipolysis and increasing energy expenditure, adipokines production | ||
[@Kidney] increasing glomerular permeability and filtration rate, antagonizing RAS activation | ||
Pro-inflammatory cytokines | ||
Anti-inflammatory cytokines | ||
[@Heart] reducing TNFα production, increasing IL-10 production, reducing infarct size | ||
Alarmins85 | [@Heart] worsening cardiac dysfunction, inducing myocardial apoptosis, fibrosis | |
Angiotensin-II91 | [@Heart] inducing cardiac hypertrophy/fibrosis, increasing expression of TNFα, IL-1 family cytokines | |
[@Skeletal Muscle] muscle wasting | ||
Lipocalin-296 | endothelial dysfunction, cardiomyocyte apoptosis |