The Impact of Diabetes Mellitus in COVID-19: A Mechanistic Review of Molecular Interactions.

Amirhossein Sahebkar,Thozhukat Sathyapalan,Habib Yaribeygi,Eusebio Chiefari,Tannaz Jamialahmadi

doi:10.1155/2020/5436832

Abstract

The ongoing pandemic of COVID-19 is now the major issue in global health. Evidence implies that patients with diabetes are at a higher risk of severe disease or death due to COVID-19 than individuals without diabetes. However, the underlying mechanism for this differential effect in individuals with and without diabetes is not clearly understood. We have reviewed the pathophysiological pathways which may facilitate the entry of virus or an increase in its infectivity in host cells in the diabetic milieu. We suggest that the preexisting pathological pathways in patients with poorly controlled diabetes increase the risk of infectivity and are responsible for the higher levels of tissue injury and death in patients with diabetes.

Highlights

Coronavirus disease 2019 (COVID-19) is an infectious disease developed by severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) [1]
While the overall rate of death is estimated to be lower than 6 percent among patients with COVID-19 disease [4], but patients with diabetes mellitus (DM) are at a higher risk [2]
Ongoing studies suggest that patients with diabetes who have poorly controlled glycemia have around four times higher death rate and longer length of hospitalization compared to patients without DM [5, 6]

Summary

Introduction

Coronavirus disease 2019 (COVID-19) is an infectious disease developed by severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) [1]. Oxidative stress activates other pathophysiologic pathways such as inflammation and necrosis and promotes downstream molecular mechanisms such as mitogen-activated protein kinase (MAPK) which intensify the progression of viral infection in the tissue [50]. Imai et al in 2008 found that severe respiratory infections due to coronaviruses are closely related to the activation of oxidative stress machinery in the cells [46].

Results

Conclusion