Not all arrestins are created equal: Therapeutic implications of the functional diversity of the β-arrestins in the heart.

Not all arrestins are created equal: Therapeutic implications of the functional diversity of the β-arrestins in the heart. World J Cardiol. 2019 Feb 26;11(2):47-56 Authors: Lymperopoulos A, Wertz SL, Pollard CM, Desimine VL, Maning J, McCrink KA Abstract The two ubiquitous, outside the retina, G protein-coupled receptor (GPCR) adapter proteins, β-arrestin-1 and -2 (also known as arrestin-2 and -3, respectively), have three major functions in cells: GPCR desensitization, i.e., receptor decoupling from G-proteins; GPCR internalization via clathrin-coated pits; and signal transduction independently of or in parallel to G-proteins. Both β-arrestins are expressed in the heart and regulate a large number of cardiac GPCRs. The latter constitute the single most commonly targeted receptor class by Food and Drug Administration-approved cardiovascular drugs, with about one-third of all currently used in the clinic medications affecting GPCR function. Since β-arrestin-1 and -2 play important roles in signaling and function of several GPCRs, in particular of adrenergic receptors and angiotensin II type 1 receptors, in cardiac myocytes, they have been a major focus of cardiac biology research in recent years. Perhaps the most significant realization coming out of their studies is that these two GPCR adapter proteins, initially thought of as functionally interchangeable, actually exert diametrically opposite effects in the mammalian myocardium....
Source: World Journal of Cardiology - Category: Cardiology Authors: Tags: World J Cardiol Source Type: research