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COVID and Cholesterol

Am J Physiol Endocrinol Metab 2020 Jul 1;319(1):E197-E202. Cholesterol: A new game player accelerating vasculopathy caused by SARS-CoV-2? Xiaoling Cao 1, Rong Yin 1, Helmut Albrecht 2 3, Daping Fan 1 4, Wenbin Tan 1 4 Abstract 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.

Hypothetical interactions among severe acute respiratory syndrome-coronavirus 2 (SARS-CoV-2), low-density lipoprotein cholesterol (LDL-c), and inflammatory cytokines in patients with coronavirus disease (COVID-19). Outline showing the proposed pathological processes of dissemination of SARS-CoV-2 and the entangled roles of LDL-c and hyperinflammation. Both SARS-CoV-2 and SARS-CoV-2-induced inflammatory cytokines regulate the biosynthesis and metabolism of LDL-c. Simultaneously, adipose tissues can be a potential reservoir for SARS-CoV-2. Inflammation- induced reactive oxygen species (ROS) signaling can facilitate the degradation of LDL-c. The increased vascular permeability by hyperinflammation can promote the LDL-c leakage into alveolar spaces.


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