Abstract
Coronavirus disease 2019 (COVID-19) may have a metabolic origin given strong links with risk factors such as lipids and glucose and co-morbidities such as obesity and type 2 diabetes mellitus. The severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) spike protein mediates viral cellular entry via the ACE2 receptor. The cytoplasmic tail of this spike protein is heavily palmitoylated. Emerging studies suggest that SARS-CoV-2 alters lipid metabolism in the lung epithelial cells by modulating peroxisome proliferator-activated receptor alpha (PPARα), possibly contributing to lipotoxicity, inflammation and untoward respiratory effects. Disruption of this process may affect palmitoylation of SARS-CoV spike protein and thus infectivity and viral assembly. COVID-19 is also increasingly being recognized as a vascular disease, with several studies noting prominent systemic endothelial dysfunction. The pathogenesis of endothelial dysfunction may also be linked to COVID-19-mediated metabolic and inflammatory effects. Herein, exercise will be compared to fenofibrate as a possible therapeutic strategy to bolster resilience against (and help manage recovery from) COVID-19. This paper will explore the hypothesis that exercise may be a useful adjuvant in a setting of COVID-19 management/rehabilitation due to its effects on PPARα and vascular endothelial function.
【저자키워드】 COVID-19, exercise, Endothelium, Vascular, PPARα, 【초록키워드】 SARS-CoV-2, Inflammation, Resilience, Coronavirus disease 2019, coronavirus, Pathogenesis, obesity, ACE2 receptor, risk factor, Spike protein, Endothelial dysfunction, co-morbidity, Alpha, receptor, therapeutic strategy, Glucose, Hypothesis, Lipid, lipid metabolism, lipotoxicity, endothelial function, Disruption, vascular disease, acute respiratory syndrome, help, SARS-CoV spike protein, cytoplasmic tail, Effect, Affect, Alter, Effects, contributing to, lung epithelial cell, increasingly, inflammatory effects, modulating, type 2 diabete, viral cellular entry,