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Loss of estrogen receptor GPER in heart cells activates the NLRP3 inflammasome, leading to heart dysfunction. Inhibiting NLRP3 in GPER-deficient mice improved heart function and reduced disease markers, suggesting a new therapeutic target for postmenopausal heart disease.

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Area of Science:

  • Cardiovascular Biology
  • Immunology
  • Endocrinology

Background:

  • Postmenopausal heart disease is linked to estrogen loss and potential immune system involvement.
  • The G-protein coupled estrogen receptor (GPER) plays a role in cardiovascular health.
  • The NLRP3 inflammasome is an innate immune system component implicated in inflammation.

Purpose of the Study:

  • To investigate the role of cardiomyocyte GPER in regulating cardiac NLRP3 inflammasome activity.
  • To determine the impact of GPER deletion on cardiac function and inflammatory pathways.
  • To explore therapeutic potential of NLRP3 inhibition in GPER-deficient hearts.

Main Methods:

  • Utilized cardiomyocyte-specific GPER knockout (KO) mice and wild-type (WT) littermates.
  • Assessed cardiac function using echocardiography and measured gene expression via RT2 Profiler PCR array.
  • Administered a NLRP3 inhibitor (MCC950) to GPER KO mice and evaluated therapeutic effects.

Main Results:

  • GPER deletion impaired cardiac systolic and diastolic function, indicated by reduced %FS, e', and increased E/e'.
  • GPER deficiency upregulated key inflammatory markers, including NLRP3 and IL-18 mRNA.
  • NLRP3 inhibition with MCC950 significantly improved cardiac function and reduced cardiac remodeling markers in GPER KO mice.

Conclusions:

  • Loss of estrogenic protection via GPER deactivation promotes cardiac dysfunction through NLRP3 inflammasome activation.
  • Targeting the NLRP3 inflammasome represents a promising therapeutic strategy for postmenopausal heart disease.
  • This study provides novel insights into the mechanisms underlying increased heart disease risk in women after menopause.