Roy B, Runa SA. SARS-CoV-2 infection and diabetes: Pathophysiological mechanism of multi-system organ failure. World J Virol 2022; 11(5): 252-274 [PMID: 36188734 DOI: 10.5501/wjv.v11.i5.252]
Corresponding Author of This Article
Bipradas Roy, MSc, PhD, Research Assistant, Department of Physiology, Wayne State University, 5374 Scott Hall, 540 E. Canfield, Detroit, MI 48201, United States. biroy@med.wayne.edu
Research Domain of This Article
Pathology
Article-Type of This Article
Review
Open-Access Policy of This Article
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/
World J Virol. Sep 25, 2022; 11(5): 252-274 Published online Sep 25, 2022. doi: 10.5501/wjv.v11.i5.252
SARS-CoV-2 infection and diabetes: Pathophysiological mechanism of multi-system organ failure
Bipradas Roy, Sadia Afrin Runa
Bipradas Roy, Department of Physiology, Wayne State University, Detroit, MI 48201, United States
Bipradas Roy, Division of Hypertension and Vascular Research, Department of Internal Medicine, Henry Ford Health System, Detroit, MI 48202, United States
Sadia Afrin Runa, Department of Biotechnology and Genetic Engineering, Bangabandhu Sheikh Mujibur Rahman Science and Technology University, Gopalganj 8100, Bangladesh
Author contributions: Roy B conceived the review design and wrote the draft; Runa SA revised the manuscript; all authors gave final approval of the version to be published.
Supported bya Predoctoral Fellowship Grant from the American Heart Association, No. 835262 (to Roy B).
Conflict-of-interest statement: All the authors report no relevant conflicts of interest for this article.
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/
Corresponding author: Bipradas Roy, MSc, PhD, Research Assistant, Department of Physiology, Wayne State University, 5374 Scott Hall, 540 E. Canfield, Detroit, MI 48201, United States. biroy@med.wayne.edu
Received: May 18, 2022 Peer-review started: May 18, 2022 First decision: June 16, 2022 Revised: June 25, 2022 Accepted: August 1, 2022 Article in press: August 1, 2022 Published online: September 25, 2022 Processing time: 128 Days and 12.4 Hours
Core Tip
Core Tip: There is no therapeutic approach yet that can eradicate diabetes and its complications from human life, as the etiopathology of diabetes is very complex. Before the outbreak of coronavirus disease 2019, it was almost unknown that diabetes is a leading risk factor that could fuel the pathogenesis of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2)-induced multi-organ dysfunction and subsequent mortality. Additionally, SARS-CoV-2-infected children and young people have been shown to develop diabetes. Therefore, identifying the precise molecular mechanisms of diabetes-induced SARS-CoV-2 susceptibility and subsequent manifestation of multi-organ dysfunction may help us to develop drugs that prevent millions of human lives.
