Related Experiment Video
Updated: Dec 20, 2025

Author Spotlight: Understanding Retinal Vessel Resilience and Disease Progression
Published on: January 12, 2024
The contribution of diabetic micro-angiopathy to adverse outcomes in COVID-19
Martin B Whyte1, Prashanth Vas2, Christian Heiss3
1Department of Clinical and Experimental Medicine, University of Surrey, United Kingdom; Department of Diabetes, King's College NHS Foundation Trust, London, United Kingdom.
Insights
Endothelial cell dysfunction is key in severe COVID-19, potentially exacerbated by hyperglycemia. Pre-existing microangiopathy in diabetes and minority groups may increase vulnerability to COVID-19 endothelitis.
Area of Science:
- Vascular Biology
- Infectious Diseases
- Endocrinology
Background:
- Endothelial cell dysfunction is increasingly recognized in severe COVID-19, contributing to microthrombi and altered vascular tone.
- Diabetes and Black, Asian, and Minority Ethnic (BAME) populations are at higher risk for adverse COVID-19 outcomes.
- Hyperglycemia, a common issue in diabetes, correlates with worse COVID-19 prognosis, but its causal role is unclear.
Purpose of the Study:
- To propose that pre-existing endothelial dysfunction, common in diabetes and BAME groups, predisposes individuals to severe COVID-19.
- To explore the link between hyperglycemia, microangiopathy, and COVID-19-associated endothelial dysfunction ('endothelitis').
Main Methods:
- This article presents a hypothesis based on existing scientific literature and evidence.
- It synthesizes findings on endothelial function, diabetes, BAME populations, hyperglycemia, and COVID-19 pathophysiology.
Main Results:
- The hypothesis suggests that underlying microangiopathy and endothelial dysfunction, prevalent in diabetes and BAME individuals, create vulnerability.
- This vulnerability may lead to more severe 'endothelitis' upon SARS-CoV-2 infection.
Conclusions:
- Pre-existing endothelial dysfunction, particularly in individuals with diabetes or from BAME backgrounds, is proposed as a key factor increasing susceptibility to severe COVID-19.
- Hyperglycemia's role as either a causative agent or a marker in this context warrants further investigation.
Abstract:
Increasing evidence points to endothelial cell dysfunction as a key pathophysiological factor in severe coronavirus disease-19 (COVID-19), manifested by platelet aggregation, microthrombi and altered vasomotor tone. This may be driven by direct endothelial cell entry by the virus, or indirectly by activated inflammatory cascade. Major risk groups identified for adverse outcomes in COVID-19 are diabetes, and those from the Black, Asian and ethnic minority (BAME) populations. Hyperglycaemia (expressed as glycated haemoglobin or mean hospital glucose) correlates with worse outcomes in COVID-19. It is not known whether hyperglycaemia is causative or is a surrogate marker - persistent hyperglycaemia is well known as an aetiological agent in microangiopathy. In this article, we propose that pre-existing endothelial dysfunction of microangiopathy, more commonly evident in diabetes and BAME groups, makes an individual vulnerable to the subsequent 'endothelitis' of COVID-19 infection.
Related Concept Videos
Pathophysiology of Diabetes
Type 1 diabetes is characterized by autoimmune-mediated destruction of pancreatic β cells, with environmental factors potentially triggering this process in genetically susceptible individuals. Despite many not having a family history, certain genes increase susceptibility,...
Diabetes Mellitus: Type 2 and Gestational
Diabetes: Symptoms, Diagnosis, and Complications
Diabetes Mellitus: Overview and Type I Subtype
Type 1 diabetes is an autoimmune disease in which the immune system mistakenly attacks and destroys the insulin-producing beta cells in the pancreas. As a result, the body is unable to produce sufficient insulin, and individuals with...
Overview of Carbohydrate Metabolism
Glucose transport into cells is facilitated by a family of transport proteins called GLUT (Glucose Transporters). GLUT4 is the primary glucose transporter for insulin-stimulated glucose...
Coronary Artery Disease I: Introduction

