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S free of relevant side effects.Relaxin Family Peptide ReceptorsThe use of relaxin for acute heart failure (defined as new onset or, more frequently, worsening of known heart failure) is promising. In the Pre-RELAX (phase II) and RELAX (phase III) trials (Teerlink et al., 2009, 2013), relaxin moderately improved dyspnea (the primary endpoint), was exceptionally safe, improved renal function, and
Et al., 2002; Zhang et al., 2005). After the demonstration of protective actions in the cardiovascular system, relaxin was tested in human heart failure. A hemodynamic pilot study in patients with stable chronic heart failure (Dschietzig et al., 2009c) demonstrated that a 24-hour intravenous infusion of recombinant human relaxin markedly elevated cardiac index without affecting heart rate and dec
T on sympathoadrenergic innervation and pacemaker cells (Cajal cells) than arterial tone (Gelman, 2008). Given the interest in the utility of vasodilators in the treatment of cardiac failure (Bhushan et al., 2014), this promises to be an important future area of research. Relaxin protects against endothelial dysfunction that denotes an inflammatory and oxidative stress-related vascular pathology
Ibrotic effects of relaxin. Relaxin-mediated increases in MMP-9 expression were also blocked by transfection of a dominant negative form of Akt or by small interfering RNA knockdown of ERK1/2, PKCz, Elk-1, c-fos, and, to a lesser extent, NFkB (Ahmad et al., 2012). This important study connects many of the known pathways of relaxin/ RXFP1 signaling to a well recognized physiologic response to rela
Ained by an incomplete understanding of the pathophysiology of scleroderma and by the enrolment of patients in the terminal stages of the disease. It is of interest to note that the dermal fibrosis of the relaxin knockout mouse is rescued by exogenous relaxin at 6 months but not rescued by administration at 12 months of age (Samuel et al., 2005). One of the interesting aspects that have emerged i

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