βArrestins in cardiac G protein-coupled receptor signaling and function: partners in crime or "good cop, bad cop"?

International Journal of Molecular Sciences
Anastasios Lymperopoulos, Shmuel Negussie

Abstract

βArrestin (βarr)-1 and -2 (βarrs) (or Arrestin-2 and -3, respectively) are universal G protein-coupled receptor (GPCR) adapter proteins expressed abundantly in extra-retinal tissues, including the myocardium. Both were discovered in the lab of the 2012 Nobel Prize in Chemistry co-laureate Robert Lefkowitz, initially as terminators of signaling from the β-adrenergic receptor (βAR), a process known as functional desensitization. They are now known to switch GPCR signaling from G protein-dependent to G protein-independent, which, in the case of βARs and angiotensin II type 1 receptor (AT1R), might be beneficial, e.g., anti-apoptotic, for the heart. However, the specific role(s) of each βarr isoform in cardiac GPCR signaling and function (or dysfunction in disease), remain unknown. The current consensus is that, whereas both βarr isoforms can desensitize and internalize cardiac GPCRs, they play quite different (even opposing in certain instances) roles in the G protein-independent signaling pathways they initiate in the cardiovascular system, including in the myocardium. The present review will discuss the current knowledge in the field of βarrs and their roles in GPCR signaling and function in the heart, focusing on the three most...Continue Reading

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Citations

Feb 11, 2014·Pflügers Archiv : European journal of physiology·Kristina LorenzFriederike Cuello
Feb 7, 2016·The International Journal of Biochemistry & Cell Biology·Anastasios LymperopoulosKatie A McCrink
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Mar 23, 2017·Journal of Cardiovascular Pharmacology·Pierre-Yves Jean-CharlesSudha K Shenoy
Aug 14, 2019·Heart Failure Reviews·Daniel Chikere AliLi Changxing

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