Publication Name	World Journal of Cardiology
Manuscript ID	29406
Country	United States

Received	2016-08-12 09:03
Peer-Review Started	2016-08-12 14:21
To Make the First Decision	2016-10-20 08:27
Return for Revision	2016-10-20 18:18
Revised	2016-11-01 01:56
Second Decision	2016-12-12 10:44
Accepted by Journal Editor-in-Chief
Accepted by Executive Editor-in-Chief	2016-12-19 10:52
Articles in Press	2016-12-19 10:52
Publication Fee Transferred
Edit the Manuscript by Language Editor
Typeset the Manuscript	2017-03-22 22:16
Publish the Manuscript Online	2017-03-26 19:18

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/
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Category	Cardiac & Cardiovascular Systems
Manuscript Type	Editorial
Article Title	Angiotensin receptor blocker drugs and inhibition of adrenal beta-arrestin-1-dependent aldosterone production: Implications for heart failure therapy
Manuscript Source	Invited Manuscript
All Author List	Anastasios Lymperopoulos and Beatrix Aukszi
Funding Agency and Grant Number
Corresponding Author	Anastasios Lymperopoulos, PhD, FAHA, FESC, Associate Professor, Department of Pharmaceutical Sciences, 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	Adrenal cortex; Adrenocortical zona glomerulosa cell; Aldosterone; Angiotensin receptor blocker; Angiotensin II type 1 receptor; β-arrestin-1; Heart failure; Suppression efficacy
Core Tip	The angiotensin II type 1 receptor (AT1R) endogenously expressed in adrenocortical cells was known for decades to induce aldosterone production via a well-defined Gq protein-mediated signaling pathway. Over the past decade, a number of studies have elucidated another, β-arrestin-1 (βarr1)-dependent signaling cascade, which proceeds in parallel to, and independently of the Gq-mediated one, and also results in aldosterone synthesis and secretion from the adrenal cortex. Importantly, although all of the Food and Drug Administration-approved angiotensin receptor blocker (ARB) drugs (AT1R antagonists) are very effective at blocking the Gq-mediated pathway, as expected, since they were designed to do so (i.e., to block the G protein signaling of the AT1R), they seem to display varying efficacies at blocking this new, βarr1-dependent pathway, which translates into significant variation at aldosterone suppression efficacies. In that context, candesartan and valsartan appear the most effective agents at blocking also the βarr1 pathway emanating from the adrenocortical AT1R, and thus, these two agents may be the best aldosterone suppressors within the ARB drug class.
Publish Date	2017-03-26 19:18
Citation	Lymperopoulos A, Aukszi B. Angiotensin receptor blocker drugs and inhibition of adrenal beta-arrestin-1-dependent aldosterone production: Implications for heart failure therapy. World J Cardiol 2017; 9(3): 200-206
URL	http://www.wjgnet.com/1949-8462/full/v9/i3/200.htm
DOI	http://dx.doi.org/10.4330/wjc.v9.i3.200

Full Article (PDF)	WJC-9-200.pdf
Full Article (Word)	WJC-9-200.doc
Manuscript File	29406-Review.doc
Answering Reviewers	29406-Answering reviewers.pdf
Audio Core Tip	29406-Audio core tip.mp3
Conflict-of-Interest Disclosure Form	29406-Conflict-of-interest statement.pdf
Copyright License Agreement	29406-Copyright assignment.pdf
Peer-review Report	29406-Peer-review(s).pdf
Scientific Misconduct Check	29406-Scientific misconduct check.pdf
Scientific Editor Work List	29406-Scientific editor work list.pdf