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G protein-coupled oestrogen receptor 1 (GPER1)/GPR30: a new player in cardiovascular and metabolic oestrogenic signalling

In English

Författare

Summary, in English

Oestrogens are important sex hormones central to health and disease in both genders that have protective effects on the cardiovascular and metabolic systems. These hormones act in complex ways via both genomic and non-genomic mechanisms. The genomic mechanisms are relatively well characterized, whereas the non-genomic ones are only beginning to be explored. Two oestrogen receptors (ER), ER alpha and ER beta, have been described that act as nuclear transcription factors but can also associate with the plasma membrane and influence cytosolic signalling. ERa has been shown to mediate both anti-atherogenic effects and pro-survival effects in pancreatic beta-cells. In recent years, a third membrane-bound ER has emerged, G protein-coupled receptor 30 or G protein-coupled oestrogen receptor 1 (GPER1), which mediates oestrogenic responses in cardiovascular and metabolic regulation. Both GPER1 knock-out models and pharmacological agents are now available to study GPER1 function. These tools have revealed that GPER1 activation may have several beneficial effects in the cardiovascular system including vasorelaxation, inhibition of smooth muscle cell proliferation, and protection of the myocardium against ischaemia/reperfusion injury, and in the metabolic system including stimulation of insulin release and protection against pancreatic beta-cell apoptosis. Thus, GPER1 is emerging as a candidate therapeutic target in both cardiovascular and metabolic disease.

Avdelning/ar

Publiceringsår

2011

Språk

Engelska

Sidor

1131-1139

Publikation/Tidskrift/Serie

British Journal of Pharmacology

Volym

163

Issue

6

Dokumenttyp

Artikel i tidskrift

Förlag

Wiley

Ämne

  • Pharmacology and Toxicology

Nyckelord

  • G protein-coupled receptor
  • oestrogen
  • cardiovascular regulation
  • metabolic regulation
  • cellular signalling
  • non-genomic mechanisms

Status

Published

Forskningsgrupp

  • Vascular Physiology
  • Drug Target Discovery

ISBN/ISSN/Övrigt

  • ISSN: 1476-5381