Cholesterol: A new game player accelerating vasculopathy caused by SARS-CoV-2?

Am J Physiol Endocrinol Metab. 2020 Jul 1;319(1):E197-E202. doi: 10.1152/ajpendo.00255.2020. Epub 2020 Jun 5.


The pandemic of coronavirus disease (COVID-19) has become a global threat to public health. Functional impairments in multiple organs have been reported in COVID-19, including lungs, heart, kidney, liver, brain, and vascular system. Patients with metabolic-associated preconditions, such as hypertension, obesity, and diabetes, are susceptible to experiencing severe symptoms. The recent emerging evidence of coagulation disorders in COVID-19 suggests that vasculopathy appears to be an independent risk factor promoting disease severity and mortality of affected patients. We recently found that the decreased levels of low-density lipoprotein cholesterols (LDL-c) correlate with disease severity in COVID-19 patients, indicating pathological interactions between dyslipidemia and vasculopothy in patients with COVID-19. However, this clinical manifestation has been unintentionally underestimated by physicians and scientific communities. As metabolic-associated morbidities are generally accompanied with endothelial cell (EC) dysfunctions, these pre-existing conditions may make ECs more vulnerable to SARS-CoV-2 attack. In this mini-review, we summarize the metabolic and vascular manifestations of COVID-19 with an emphasis on the association between changes in LDL-c levels and the development of severe symptoms as well as the pathophysiologic mechanisms underlying the synergistic effect of LDL-c and SARS-CoV-2 on EC injuries and vasculopathy.

Keywords: COVID-19; LDL; SARS-CoV-2; endothelial cells; hypertension; obesity; thrombosis; vasculopathy.

Publication types

  • Research Support, N.I.H., Extramural
  • Comment

MeSH terms

  • Betacoronavirus
  • COVID-19
  • China
  • Cholesterol
  • Coronavirus Infections*
  • Coronavirus*
  • Humans
  • Pandemics*
  • Pneumonia, Viral*
  • SARS Virus*
  • SARS-CoV-2


  • Cholesterol