“…In a similar model, relaxin decreases inflammatory cytokines, counteracts oxidative damage by increasing SOD-1 and SOD-2 expression, and ameliorates neutrophil-related injury as assessed by myeloperoxidase levels (Collino et al, 2013). Finally, the beneficial effects of relaxin are also observed in IR experiments in isolated rat lungs (Alexiou et al, 2010(Alexiou et al, , 2013 where there is inhibition of leukocytes and oxidative surge, as well as prevention of ET-1 stimulation, resulting in less edema formation and lower pulmonary vascular pressure.…”
mentioning
confidence: 94%
“…NO appears to be critically involved in organ protection (Masini et al, 1997;Alexiou et al, 2010Alexiou et al, , 2013Collino et al, 2013). In rat lung, relaxin evokes an early and moderate increase in iNOS dependent on ERK1/2 activation that is counterbalanced by PI3K recruitment (Alexiou et al, 2013).…”
“…In a similar model, relaxin decreases inflammatory cytokines, counteracts oxidative damage by increasing SOD-1 and SOD-2 expression, and ameliorates neutrophil-related injury as assessed by myeloperoxidase levels (Collino et al, 2013). Finally, the beneficial effects of relaxin are also observed in IR experiments in isolated rat lungs (Alexiou et al, 2010(Alexiou et al, , 2013 where there is inhibition of leukocytes and oxidative surge, as well as prevention of ET-1 stimulation, resulting in less edema formation and lower pulmonary vascular pressure.…”
mentioning
confidence: 94%
“…NO appears to be critically involved in organ protection (Masini et al, 1997;Alexiou et al, 2010Alexiou et al, , 2013Collino et al, 2013). In rat lung, relaxin evokes an early and moderate increase in iNOS dependent on ERK1/2 activation that is counterbalanced by PI3K recruitment (Alexiou et al, 2013).…”
“…Several strategies have been assessed to reduce I/R injury and to enhance organ preservation, including adding a range of chemical compounds, or genetic modification of the organ with the adenovirus delivery system. 8,9 Some organ preservation solutions have been developed and applied in transplantation, but cold ischemic storage of the heart is still limited to 4 to 6 hours because preservation solutions have been unable to significantly inhibit the ensuing I/R injury. 10 Cx43, as an important player in the pathophysiology of myocardial I/R injury, has a role in protection during ischemic and pharmacologic pre-conditioning.…”
“…72 In addition to the heart, relaxin protects against ischemia-reperfusion injury in other organs including kidney, lung, liver, brain, and intestine. [91][92][93][94][95][96] A feature that contributes to the morbidity and mortality in heart disease is cardiac fibrosis. 97 One of the best characterized functions of relaxin is in remodeling of extracellular matrix proteins and protection from fibrosis.…”
Acute heart failure remains an enormous health concern worldwide, and is a major cause of death and hospitalization. In spite of this, the treatment strategies for acute heart failure have remained largely unchanged for the past 2 decades. Several large randomized, placebocontrolled clinical trials have recently been conducted to attempt to improve the treatment and outcomes of acute decompensated heart failure. Some studies, including the EVEREST (tolvaptan) and ASCEND (nesiritide) showed efficacy at relieving early symptoms, but failed to improve long-term outcomes. Others, including PROTECT (rolofylline) and ASTRONAUT (aliskiren) showed little benefit in the relief of early symptoms or long-term outcomes. The recent RELAX-AHF studies using serelaxin, a recombinant form of relaxin, have shown considerable promise. Importantly, serelaxin improved congestion (dyspnea) and other early targets of acute decompensated heart failure treatment, but also improved mortality at 180 days. The purpose of this review is to provide an overview of current treatment strategies for acute decompensated heart failure, and a discussion of the recent clinical trials, with an emphasis on the serelaxin studies.
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