Cardiovascular Dysfunction in COVID-19: Association Between Endothelial Cell Injury and Lactate
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Published on: May 28, 2019
Kun Yang1,2, Matthew Holt3, Min Fan1,2
1Department of Surgery, James H. Quillen College of Medicine, East Tennessee State University, Johnson City, TN, United States.
Insights
Severe Acute Respiratory Syndrome Coronavirus-2 (SARS-CoV-2) infection causes endothelial cell injury, a key factor in COVID-19 severity. This review explores cardiovascular damage, metabolic changes, and lactate's potential role in SARS-CoV-2-induced endothelial dysfunction.
Area of Science:
- Cardiovascular Medicine
- Infectious Diseases
- Metabolic Processes
Background:
- Coronavirus disease 2019 (COVID-19), caused by Severe Acute Respiratory Syndrome Coronavirus-2 (SARS-CoV-2), is a global health crisis.
- Endothelial cell damage is increasingly recognized as a critical factor in COVID-19 pathogenesis, severity, and mortality.
- Metabolic alterations are closely linked to the pathogenesis of infectious diseases, including COVID-19.
Purpose of the Study:
- To review cardiovascular injuries associated with SARS-CoV-2 infection.
- To examine metabolic alterations in COVID-19 patients.
- To propose lactate as a potential mediator of endothelial cell injury in COVID-19.
Main Methods:
- Literature review of emerging evidence on COVID-19 pathogenesis.
- Analysis of studies linking metabolic processes to infectious diseases.
- Exploration of lactate's role in endothelial barrier function.
Main Results:
- SARS-CoV-2 infection can lead to significant cardiovascular injuries.
- Metabolic dysregulation is a common feature in COVID-19.
- Lactate has been identified as a potential biomarker and mediator of endothelial barrier dysfunction.
Conclusions:
- Endothelial cell damage is a central mechanism in COVID-19.
- Metabolic alterations, particularly involving lactate, may contribute to COVID-19 severity.
- Further research is warranted to elucidate the role of lactate in SARS-CoV-2-induced endothelial injury.
Abstract:
Coronavirus disease 2019 (COVID-19), an infectious respiratory disease propagated by a new virus known as Severe Acute Respiratory Syndrome Coronavirus-2 (SARS-CoV-2), has resulted in global healthcare crises. Emerging evidence from patients with COVID-19 suggests that endothelial cell damage plays a central role in COVID-19 pathogenesis and could be a major contributor to the severity and mortality of COVID-19. Like other infectious diseases, the pathogenesis of COVID-19 is closely associated with metabolic processes. Lactate, a potential biomarker in COVID-19, has recently been shown to mediate endothelial barrier dysfunction. In this review, we provide an overview of cardiovascular injuries and metabolic alterations caused by SARS-CoV-2 infection. We also propose that lactate plays a potential role in COVID-19-driven endothelial cell injury.
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