Improvement of the Immunity System Through Sports: Novel Regulatory Mechanisms for Hypertension

Figures

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  Fig. 1.. The role of immune cells in hypertensive inflammation. ET-1, (endothelin, ET)-1; DAMPs, damage-associated molecular patterns; PAMPs, pathogen-associated molecular patterns; BP, blood pressure; eNOS, endothelial nitric oxide synthase; α2Ars, α2-adrenergic receptors; NETs, neutrophil extracellular traps; VSMCs, vascular smooth muscle cells; Flt3L, fms-like tyrosine kinase 3 ligands; Treg, regulatory T cells; NK cell, natural killer cell; NF-κB, nuclear factor kappa-B; Th17, T helper cell 17; Ang II, angiotensin II; IFN-γ, interferon-γ; TNF-α, tumor necrosis factor-α; IL-10, interleukin-10; TGF-β, transforming growth factor-β.

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  Fig. 2.. Exercise training reduces hypertension and targets organ damage by regulating the immune system. (A) The relationship between exercise training and immune system. (B) The mechanism of action of exercise training on different immune cells. (C) Exercise training regulates the mechanism of hypertension through the immune system. Flt3L, fms-like tyrosine kinase 3 ligands; NETs, neutrophil extracellular traps; NK cell, natural killer cell; CCR2, chemokine receptor 2; M1, macrophages; M2, macrophages; Treg, regulatory T cells; RAAS, renin-angiotensin-aldosterone system; Th17, T helper cell 17.