Abstract
The present review describes COVID-19 severity in diabetes and diabetic kidney disease. We discuss the crucial effect of COVID-19-associated cytokine storm and linked injuries and associated severe mesenchymal activation in tubular epithelial cells, endothelial cells, and macrophages that influence neighboring cell homeostasis, resulting in severe proteinuria and organ fibrosis in diabetes. Altered microRNA expression disrupts cellular homeostasis and the renin-angiotensin-system, targets reno-protective signaling proteins, such as angiotensin-converting enzyme 2 (ACE2) and MAS1 receptor (MAS), and facilitates viral entry and replication in kidney cells. COVID-19-associated endotheliopathy that interacts with other cell types, such as neutrophils, platelets, and macrophages, is one factor that accelerates prethrombotic reactions and thrombus formation, resulting in organ failures in diabetes. Apart from targeting vital signaling through ACE2 and MAS, severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infections are also associated with higher profibrotic dipeptidyl transferase-4 (DPP-4)-mediated mechanisms and suppression of AMP-activated protein kinase (AMPK) activation in kidney cells. Lowered DPP-4 levels and restoration of AMPK levels are organ-protective, suggesting a pathogenic role of DPP-4 and a protective role of AMPK in diabetic COVID-19 patients. In addition to standard care provided to COVID-19 patients, we urgently need novel drug therapies that support the stability and function of both organs and cell types in diabetes.
Highlights
Coronavirus disease 2019 (COVID-19) is caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), a beta-coronavirus that belongs to the family Coronaviridae and order Nidovirales [1]
We focus on the mechanisms by which COVID-19 influences diabetes and diabetic kidney disease (DKD)
It has been shown that SARS-CoV-2 affects the kidneys and causes podocyte injury that leads to proteinuria and release of proinflammatory cytokines and chemokines, including transforming-growth factor-β (TGF-β), Interferon gamma, interleukins, vascular endothelial growth factors (VEGF), platelet-derived growth factor (PDGF), and chemokine ligand 1 (CXCL1), that causes glomerular sclerosis, hyalinosis, mesangial matrix deposition, and fibrosis [57]
Summary
Coronavirus disease 2019 (COVID-19) is caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), a beta-coronavirus that belongs to the family Coronaviridae and order Nidovirales [1]. From the onset of COVID-19, a relationship between the clinical course of severe acute respiratory syndrome (SARS) and blood glucose levels has been established Patients with both diabetes and COVID-19 infection can be harder to treat, due to fluctuations in blood glucose levels, and possibly, the presence of other related complications. Yang et al reported that lymphocytopenia occurs in more than 80% of critically ill patients with COVID-19 [15], and is a prominent feature because SARS-CoV infection damages the cytoplasmic component of the lymphocyte and destroys the cell [13,16]. We focus on the mechanisms by which COVID-19 influences diabetes and diabetic kidney disease (DKD)
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