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. 2016 Jul 12;7:195. doi: 10.3389/fphar.2016.00195

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Copyright © 2016 Wetzl, Schinner, Kees, Hofmann, Faerber and Schlossmann.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Proposed hypothesis for in vivo antifibrotic signaling pathway of serelaxin in kidney. Serelaxin mediates its antifibrotic effect via RXFP1/cGMP/cGKI to inhibit TGF-β dependent Smad- and ERK-phosphorylation, which subsequently decreases ECM accumulation and suppresses profibrotic stimuli; α-SMA, α-smooth muscle actin; cGKI, cGMP-dependent protein kinase I; cGMP, cyclic guanosine monophosphate; CTGF, connective tissue growth factor; ECM, extracellular matrix; ERK, extracellular-signal regulated kinase; GMP, guanosine monophosphate; MMPs, matrix metalloproteinases; PDE5a, phosphodiesterase 5a; RXFP1, relaxin family peptide receptor 1; Smad, small mothers against decapentaplegic protein; TGF-β, transforming growth factor-β.