ISSN |
1949-8462 (online) |
Open Access |
This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/ |
Copyright |
© The Author(s) 2019. Published by Baishideng Publishing Group Inc. All rights reserved. |
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Publisher |
Baishideng Publishing Group Inc, 7041 Koll Center Parkway, Suite 160, Pleasanton, CA 94566, USA |
Website |
http://www.wjgnet.com |
Category |
Cardiac & Cardiovascular Systems |
Manuscript Type |
Editorial |
Article Title |
Not all arrestins are created equal: Therapeutic implications of the functional diversity of the β arrestins in the heart
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Manuscript Source |
Invited Manuscript |
All Author List |
Anastasios Lymperopoulos, Shelby L Wertz, Celina M Pollard, Victoria L Desimine, Jennifer Maning and Katie A McCrink |
Funding Agency and Grant Number |
Funding Agency |
Grant Number |
NSU’s President’s Faculty Research and Development Grant (PFRDG) |
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Corresponding Author |
Anastasios Lymperopoulos, BPharm, FAHA, MSc, PhD, Associate Professor, Research Associate, Laboratory for the Study of Neurohormonal Control of the Circulation, Department of Pharmaceutical Sciences (Pharmacology), College of Pharmacy, Nova Southeastern University, 3200 S. University Dr., HPD (Terry) Bldg/Room 1338, Fort Lauderdale, FL 33328, United States. al806@nova.edu |
Key Words |
Adverse remodeling; β arrestin; Biased signaling; Cardiac myocyte; Cardiac fibroblast; contractility; Functional divergence; G protein-coupled receptor; Heart failure; Hormone; Myocardial infarction; Signal transducer |
Core Tip |
Presumed functionally similar for a long time, we now know that the two β arrestins display significant functional diversity in several organs and tissues, including in the cardiovascular system. Their functional distinction also in the mammalian heart has been clearly documented over the past few years. β arrestin-1, which is far more abundant than β arrestin-2 in almost every tissue including the myocardium, opposes the cyclic adenosine monophosphate (cAMP)-dependent pro-contractile signaling of the β1 adrenergic receptor (β1AR), and promotes cardiac apoptosis, inflammation, and other adverse remodeling-associated processes post-myocardial infarction. Conversely, β arrestin-2 promotes catecholamine-dependent cardiac contractility directly, via SERCA2a potentiation, and indirectly, by leaving β1AR’s cAMP-dependent pro-contractile signaling unaffected. |
Publish Date |
2019-02-25 03:36 |
Citation |
Lymperopoulos A, Wertz SL, Pollard CM, Desimine VL, Manning J, McCrink KA. Not all arrestins are created equal: Therapeutic implications of the functional diversity of the β arrestins in the heart. World J Cardiol 2019; 11(2): 47-56 |
URL |
https://www.wjgnet.com/1949-8462/full/v11/i2/47.htm |
DOI |
https://dx.doi.org/10.4330/wjc.v11.i2.47 |