Publication Name	World Journal of Cardiology
Manuscript ID	67240
Country	United States

Received	2021-04-19 04:42
Peer-Review Started	2021-04-19 04:45
To Make the First Decision
Return for Revision	2021-07-08 07:13
Revised	2021-08-02 20:08
Second Decision	2021-11-30 03:43
Accepted by Journal Editor-in-Chief
Accepted by Executive Editor-in-Chief	2021-11-30 19:12
Articles in Press	2021-11-30 19:12
Publication Fee Transferred
Edit the Manuscript by Language Editor
Typeset the Manuscript	2021-12-21 07:11
Publish the Manuscript Online	2021-12-23 06:10

ISSN	1949-8462 (online)
Open Access	This article is an open-access article that was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution NonCommercial (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: https://creativecommons.org/Licenses/by-nc/4.0/
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Category	Cardiac & Cardiovascular Systems
Manuscript Type	Review
Article Title	Cardiovascular benefits from SGLT2 inhibition in type 2 diabetes mellitus patients is not impaired with phosphate flux related to pharmacotherapy
Manuscript Source	Invited Manuscript
All Author List	Mouhamed Nashawi, Mahmoud S Ahmed, Toka Amin, Mujahed Abualfoul and Robert Chilton
Funding Agency and Grant Number
Corresponding Author	Mouhamed Nashawi, MD, Academic Research, Staff Physician, Department of Internal Medicine, Baylor Scott and White All Saints Medical Center, 1400 8th Ave, Fort Worth, TX 76132, United States. nashawi@livemail.uthscsa.edu
Key Words	Sodium-glucose cotransporter 2; Phosphate; Hyperphosphatemia; Cardiovascular; Canagliflozin; Dapagliflozin; Empagliflozin; Endothelial
Core Tip	Sodium-glucose cotransporter 2 (SGLT2) inhibitors have received increased attention regarding their pleiotropic effects given their markedly impressive performance in cardiovascular outcome trials (CVOT). Preliminary evidence shows that their role as antidiabetic agents is not their sole mechanism in achieving these cardiorenal protective properties. Therefore, investigation in the auxiliary properties that they hold concomitant with glucose control, vindicated by not only CVOTs, but meta-analyses, retrospective studies, and case reports has led to increased interest in delineating their global pharmacodynamic effects across the spectrum of gene expression and molecular modulation to end-organ translational biology. Such a full profile of their effects is not yet understood given the refractory period between clinical evidence supporting their utilization and a proclivity for their implementation in practical clinical environments. In this review, we answer inquiries regarding how via a multifarious avenues, SGLT2 inhibitors, while carrying a negative effect of induced phosphatemia (which is deleterious to the heart), compensate for this phenomenon, retaining their propensity for net cardiac benefit upon pharmacotherapeutic administration under appropriate clinical circumstances.
Publish Date	2021-12-23 06:10
Citation	Nashawi M, Ahmed MS, Amin T, Abualfoul M, Chilton R. Cardiovascular benefits from SGLT2 inhibition in type 2 diabetes mellitus patients is not impaired with phosphate flux related to pharmacotherapy. World J Cardiol 2021; 13(12): 676-694
URL	https://www.wjgnet.com/1949-8462/full/v13/i12/676.htm
DOI	https://dx.doi.org/10.4330/wjc.v13.i12.676

Full Article (PDF)	WJC-13-676.pdf
Full Article (Word)	WJC-13-676.docx
Manuscript File	67240_Auto_Edited-YJM.docx
Answering Reviewers	67240-Answering reviewers.pdf
Audio Core Tip	67240-Audio core tip.m4a
Conflict-of-Interest Disclosure Form	67240-Conflict-of-interest statement.pdf
Copyright License Agreement	67240-Copyright license agreement.pdf
Peer-review Report	67240-Peer-review(s).pdf
Scientific Misconduct Check	67240-Bing-Liu M-1.png
Scientific Editor Work List	67240-Scientific editor work list.pdf
CrossCheck Report	67240-CrossCheck report.pdf