Coronavirus Disease (COVID)-19 and Diabetic Kidney Disease.
Swayam Prakash SrivastavaRohit SrivastavaSubhash ChandJulie Elizabeth GoodwinPublished in: Pharmaceuticals (Basel, Switzerland) (2021)
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.
Keyphrases
- sars cov
- respiratory syndrome coronavirus
- coronavirus disease
- type diabetes
- protein kinase
- angiotensin converting enzyme
- cardiovascular disease
- angiotensin ii
- induced apoptosis
- glycemic control
- single cell
- endothelial cells
- cell therapy
- skeletal muscle
- cell cycle arrest
- stem cells
- wound healing
- poor prognosis
- early onset
- bone marrow
- emergency department
- binding protein
- drug delivery
- weight loss
- long non coding rna
- endoplasmic reticulum stress
- cell death
- quality improvement
- metabolic syndrome
- oxidative stress
- drug induced
- electronic health record
- liver fibrosis