期刊
FRONTIERS IN IMMUNOLOGY
卷 13, 期 -, 页码 -出版社
FRONTIERS MEDIA SA
DOI: 10.3389/fimmu.2022.868679
关键词
COVID-19; aerobic glycolytic metabolism; lactate; endothelial cell; cardiovascular dysfunction; HMGB1 (High mobility group box 1); thrombosis; vascular permeability
类别
资金
- National Institutes of Health [HL071837, HL153270, GM083016, GM119197]
- American Heart Association Postdoctoral Fellowship [916710, C06RR0306551]
COVID-19, caused by SARS-CoV-2, results in global healthcare crises. Endothelial cell damage and lactate play important roles in COVID-19 pathogenesis and severity.
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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