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Published on: November 5, 2021
Cholesterol: A new game player accelerating vasculopathy caused by SARS-CoV-2?
Xiaoling Cao1, Rong Yin1, Helmut Albrecht2,3
1Department of Cell Biology and Anatomy, School of Medicine, University of South Carolina, Columbia, South Carolina.
Coronavirus disease (COVID-19) impacts multiple organs, especially in patients with metabolic conditions. This review highlights how low-density lipoprotein cholesterol (LDL-c) changes and endothelial cell (EC) dysfunction worsen COVID-19 severity and vascular damage.
Area of Science:
- Cardiovascular Medicine
- Infectious Diseases
- Metabolic Disorders
Background:
- COVID-19 causes multi-organ dysfunction, including vascular damage.
- Metabolic conditions like obesity and diabetes increase COVID-19 severity.
- Coagulation disorders and vasculopathy are linked to COVID-19 mortality.
Purpose of the Study:
- To review metabolic and vascular manifestations of COVID-19.
- To emphasize the link between low-density lipoprotein cholesterol (LDL-c) levels and COVID-19 severity.
- To explore pathophysiologic mechanisms of LDL-c and SARS-CoV-2 on endothelial cells (ECs).
Main Methods:
- Literature review of metabolic and vascular aspects of COVID-19.
- Analysis of existing evidence on LDL-c levels in COVID-19 patients.
- Exploration of pathophysiologic mechanisms involving ECs, LDL-c, and SARS-CoV-2.
Main Results:
- Decreased LDL-c levels correlate with increased COVID-19 disease severity.
- Metabolic conditions may predispose ECs to SARS-CoV-2 attack.
- Synergistic effects of LDL-c and SARS-CoV-2 contribute to EC injury and vasculopathy.
Conclusions:
- Dyslipidemia, particularly altered LDL-c, is a significant factor in COVID-19 vasculopathy.
- Endothelial cell dysfunction is a key mechanism linking metabolic issues to severe COVID-19.
- Further research is needed to understand and address the metabolic and vascular complications of COVID-19.
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