Impaired left-ventricular cardiac function in male GPR30-deficient mice.

نویسندگان

  • Martina Delbeck
  • Stefan Golz
  • Richardus Vonk
  • Wiebke Janssen
  • Tim Hucho
  • Jörg Isensee
  • Stefan Schäfer
  • Christiane Otto
چکیده

G-protein-coupled receptor 30 (GPR30) has been reported to act as a membrane-bound estrogen receptor that is involved in the mediation of non-genomic estradiol signalling. In this study, we demonstrated that male, but not female, GPR30-deficient mice suffer from impaired left‑ventricular cardiac function. Left ventricles from male mutant mice were enlarged. There were no malformations in the valves or outflow tract of the heart. Both the contractility and relaxation capacity of the left ventricle were reduced, leading to increased left‑ventricular end-diastolic pressure in GPR30-deficient mice. In conclusion, our data support a role for GPR30 in the gender-specific aspects of heart failure.

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عنوان ژورنال:
  • Molecular medicine reports

دوره 4 1  شماره 

صفحات  -

تاریخ انتشار 2011