Inhibitory effects of relaxin on cardiac fibroblast-to-myofibroblast transition: an electrophysiological study

Experimental Physiology
Roberta SqueccoFabio Francini

Abstract

What is the central question of this study? Fibroblast-to-myofibroblast transition is a key mechanism in the reparative response to tissue damage, but myofibroblast persistence in the wound leads to fibrosis and organ failure. The role of relaxin as an antifibrotic agent capable of counteracting the acquisition of biophysical features of differentiated myofibroblasts deserves further investigation. What is the main finding and its importance? Electrophysiological analysis showed that relaxin, administered during profibrotic treatment, hyperpolarizes the membrane potential and attenuates delayed rectifier and inwardly rectifying K(+) currents, which usually increase in the transition to myofibroblasts. These findings provide further clues to the therapeutic potential of relaxin in fibrosis. The hormone relaxin (RLX) is produced by the heart and may be involved in endogenous mechanisms of cardiac protection against ischaemic injury and fibrosis. Recent findings in cultured cardiac stromal cells suggest that RLX can inhibit fibroblast-to-myofibroblast transition, thereby counteracting fibrosis. In order to explore its efficiency as an antifibrotic agent further, we designed the present study to investigate whether RLX may influenc...Continue Reading

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Citations

Jun 25, 2016·Nature Reviews. Drug Discovery·Robert G GourdiePeter Kohl
Jun 3, 2016·British Journal of Pharmacology·C S SamuelR G Bennett
Apr 21, 2017·Frontiers in Pharmacology·Silvia NistriDaniele Bani
Mar 2, 2018·World Journal of Gastroenterology : WJG·Eglantina IdrizajMaria Caterina Baccari

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