Relaxin is a hormone of pregnancy first discovered for its ability to induce ligament relaxation in nonpregnant guinea pig and is important for softening of the birth canal during parturition, decidualization, implantation, nipple development and increased maternal renal perfusion, glomerular filtration, and cardiac output. Subsequently, relaxin has been shown to exert multiple beneficial cardiovascular effects during pathological events such as hypertension, atrial fibrillation, heart failure and myocardial infarction, including suppression of arrhythmia and inflammation, and reversal of fibrosis. Despite extensive studies, the mechanisms underlying relaxin's effects are not well understood. Relaxin signals primarily through its G protein coupled receptor, the relaxin family peptide receptor-1, to activate multiple signaling pathways and this review summarizes our understanding of these pathways as they relate to the cardioprotective actions of relaxin, focusing on relaxin's anti-fibrotic, anti-arrhythmic and anti-inflammatory properties. Further, this review includes a brief overview of relaxin in clinical trials for heart failure and progress in the development of relaxin mimetics.
Keywords: Fibrosis; RLX; RLX receptor; RXFP1; Relaxin.
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