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Monitoring Changes in Human Umbilical Vein Endothelial Cells upon Viral Infection Using Impedance-Based Real-Time Cell Analysis
Published on: May 5, 2023
Endothelial activation and dysfunction in metabolic syndrome, type 2 diabetes and coronavirus disease 2019
Melvin R Hayden1,2,3
1Department of Internal Medicine, University of Missouri-Columbia School of Medicine, Camdenton, Missouri, USA.
Insights
Type 2 diabetes mellitus (T2DM) exacerbates COVID-19 severity by damaging blood vessels and endothelial cells. Understanding these links is crucial for managing diabetic patients during the pandemic.
Area of Science:
- Cardiovascular Science
- Infectious Diseases
- Endocrinology
Background:
- COVID-19, caused by SARS-CoV-2, presents increased risks for older individuals, males, and those with comorbidities like cardiovascular disease, diabetes, and smoking.
- Type 2 Diabetes Mellitus (T2DM) is an age-related condition characterized by metabolic dysfunction, including insulin resistance, hyperglycemia, and endothelial issues.
- Endothelial cell activation and dysfunction are increasingly recognized as critical factors in both T2DM and severe COVID-19 outcomes.
Purpose of the Study:
- To review the intricate relationship between endothelial cell activation and dysfunction in the context of Type 2 Diabetes Mellitus (T2DM) and COVID-19.
- To elucidate how COVID-19 may exacerbate pre-existing vascular vulnerabilities in patients with T2DM.
- To highlight the importance of understanding the intersection of T2DM and COVID-19 for global health strategies.
Main Methods:
- This is a review article, synthesizing existing research on COVID-19 pathophysiology and T2DM.
- The review focuses on the impact of both conditions on endothelial cells and vascular integrity.
- Literature analysis was conducted to evaluate the intersection of T2DM-related endothelial dysfunction and COVID-19-induced vascular injury.
Main Results:
- COVID-19 causes significant injury to the respiratory system's microvasculature, including the alveolar blood-gas barrier.
- The virus can unmask and worsen pre-existing endothelial damage in T2DM patients, affecting the endothelial glycocalyx and leading to macro/microvascular complications.
- T2DM shares common pathways with COVID-19 that promote endothelial activation and dysfunction, contributing to severe disease.
Conclusions:
- T2DM significantly increases morbidity and mortality in COVID-19 patients due to shared pathways of endothelial dysfunction.
- COVID-19 exacerbates the vascular complications inherent in T2DM, leading to multi-organ damage.
- Further research is essential to understand and mitigate the heightened risks faced by diabetic individuals infected with SARS-CoV-2.
Abstract:
The novel coronavirus disease 2019 (COVID-19) caused by severe acute respiratory syndrome coronavirus-2 infection is a serious global concern. Increased morbidity and mortality is associated with older age, male gender, cardiovascular disease, diabetes, and smoking. As COVID-19 spreads from coastal borders, both state to state and country to country, our understanding of its pathophysiology has evolved. Age and type 2 diabetes mellitus (T2DM) play especially important roles in COVID-19 progression. T2DM is an age-related disease associated with metabolic syndrome, obesity, insulin resistance (hyperinsulinemia), hyperlipidemia, hypertension, hyperglycemia, and endothelial activation and dysfunction. This review evaluates the relationships and intersection between endothelial cell activation and dysfunction in T2DM and COVID-19. COVID-19 induces multiple injuries of the terminal bronchioles and alveolar blood-gas barrier and associated ultrastructural tissue remodeling. COVID-19 may unmask multiple vulnerabilities associated with T2DM including damage to the endothelial glycocalyx and multiple end-organ macro and microvascular diseases. Unmasking existing vulnerabilities in diabetic patients with COVID-19 is important. Globally, we must come together to better understand why T2DM is associated with increased COVID-19 morbidity and mortality.
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