Anti-atherosclerotic effects of serelaxin in apolipoprotein E-deficient mice

Serelaxin treatment reverses vascular dysfunction and left ventricular hypertrophy in a mouse model of Type 1 diabetes

“…For instance, serelaxin decreased NOX activity and oxidative markers in the kidney of Ang II-induced hypertensive rats4243. Serelaxin also reduced AT 1 R expression in the aorta of ApoE −/− mice, which was associated with a reduction in superoxide production44. In the present study, serelaxin could suppress diabetes-induced hyper-responsiveness to Ang II in a similar fashion.…”

Relaxin-2 in Cardiometabolic Diseases: Mechanisms of Action and Future Perspectives

“…Thus, and although little is known so far, the proved effect of relaxin on regulating endothelial function suggests that relaxin could also ameliorate the inflammatory response in the vascular system under pathological conditions, and this opens a promising new field of study of relaxin regarding its potential role as a regulator of cardiovascular inflammation. In fact, in human endothelium and vascular smooth muscle cells, relaxin was already proved as a potent inhibitor of early vascular inflammation, decreasing the expression of endothelial adhesion molecules, cytokine expression and suppressing monocyte adhesion to the endothelium (Brecht et al, 2011 ), a result also observed in vivo in female apolipoprotein E-deficient mice fed with a high-fat and cholesterol-rich diet for 6 weeks, in which relaxin treatment for the last 4 weeks reduced vascular oxidative stress, improved endothelium-dependent vasodilatation, reduced the development of the atherosclerotic plaque, decreased circulating concentrations of the cytokines interleukin (IL)-6 and IL-10, and down-regulated the angiotensin II type 1a receptor in the aorta, but in this study authors did not find differences in vascular macrophage, T-cell or neutrophil infiltration, nor in collagen/vascular smooth muscle cell content between relaxin treated and control mice (Tiyerili et al, 2016 ).…”

Short‐term (48 hours) intravenous serelaxin infusion has no effect on myogenic tone or vascular remodeling in rat mesenteric arteries

“…Specifically, AT 1a and AT 2 receptors and Ren were upregulated but not AT 1b receptors. Recent work reported that 4 weeks of sRLX treatment in apolipoprotein E knockout mice reduced AT 1 receptor expression in the aorta, illustrating different effects of long‐ vs short‐term sRLX treatment. We have also shown that sRLX suppresses diabetes‐induced increases in Agt II‐induced contraction and speculated that these effects are mediated, in part, through heterodimer formation between RXFP1 and AT 2 receptors, hence counteracting the effects of AT 1 receptors in mediating vasoconstriction.…”