PLoS ONE (Jan 2012)

(Pro)renin receptor triggers distinct angiotensin II-independent extracellular matrix remodeling and deterioration of cardiac function.

  • Anne-Mari Moilanen,
  • Jaana Rysä,
  • Raisa Serpi,
  • Erja Mustonen,
  • Zoltán Szabò,
  • Jani Aro,
  • Juha Näpänkangas,
  • Olli Tenhunen,
  • Meeri Sutinen,
  • Tuula Salo,
  • Heikki Ruskoaho

DOI
https://doi.org/10.1371/journal.pone.0041404
Journal volume & issue
Vol. 7, no. 7
p. e41404

Abstract

Read online

BackgroundActivation of the renin-angiotensin-system (RAS) plays a key pathophysiological role in heart failure in patients with hypertension and myocardial infarction. However, the function of (pro)renin receptor ((P)RR) is not yet solved. We determined here the direct functional and structural effects of (P)RR in the heart.Methodology/principal findings(P)RR was overexpressed by using adenovirus-mediated gene delivery in normal adult rat hearts up to 2 weeks. (P)RR gene delivery into the anterior wall of the left ventricle decreased ejection fraction (PConclusions/significanceThese results indicate for the first time that (P)RR triggers distinct Ang II-independent myocardial fibrosis and deterioration of cardiac function in normal adult heart and identify (P)RR as a novel therapeutic target to optimize RAS blockade in failing hearts.