Jennifer Ghandour

TL;DR: In this article, the authors investigated whether GPCR-kinase-2 and -5 phosphorylates and inhibits the mineralocorticoid receptor (MR) but also activates the G protein-coupled estrogen receptor (GPER) in the heart.

TL;DR: It is suggested that adrenal GRK2 may be a molecular link connecting the sympathetic nervous and renin-angiotensin systems at the level of the adrenal cortex and that its inhibition might be therapeutically advantageous in hyperaldosteronism-related conditions.

TL;DR: Adrenal βarrestin1 upregulation is one of the mechanisms by which tobacco compounds, like nicotine, promote cardio-toxic hyperaldosteronism in vitro and in vivo, and represents a novel therapeutic target for tobacco-related heart disease prevention or mitigation.

TL;DR: It is found that carvedilol, but not metoprolol, acutely induces βarrestin2 interaction with SERCA2a in H9c2 cardiomyocytes and in neonatal rat ventricular myocytes (NRVMs), resulting in enhanced SERCA1a SUMOylation and activity, which translates into enhanced SERca2a activity only in the presence of the β2AR-selective inverse agonist ICI 118,551 (ICI).

TL;DR: In this paper , the authors examined whether Regulator of G protein Signaling (RGS)-4 regulates cardiac FFAR3 signaling and found that RGS4 is essential for dampening of propionate/FFAR3-dependent signaling in H9c2 cardiomyocytes since siRNA-mediated RGS 4 depletion significantly enhances the effect of propionic acid on cAMP lowering, Gi/o activation, and p38 MAPK activation.