Abstract
The current Coronavirus disease 2019 (COVID-19) pandemic has become a global challenge. Managing a large number of acutely ill patients in a short time, whilst reducing the fatality rate and dealing with complications, brings unique difficulties. The most striking pathophysiological features of patients with severe COVID-19 are dysregulated immune responses and abnormal coagulation function, which can result in multiple-organ failure and death. Normally metabolized high-density lipoprotein (HDL) performs several functions, including reverse cholesterol transport, direct binding to lipopolysaccharide (LPS) to neutralize LPS activity, regulation of inflammatory response, anti-thrombotic effects, antioxidant, and anti-apoptotic properties. Clinical data shows that significantly decreased HDL levels in patients with COVID-19 are correlated with both disease severity and mortality. However, the role of HDL in COVID-19 and its specific mechanism remain unclear. In this analysis, we review current evidence mainly in the following areas: firstly, the pathophysiological characteristics of COVID-19, secondly, the pleiotropic properties of HDL, thirdly, the changes and clinical significance of HDL in COVID-19, and fourthly the prospect of HDL-targeting therapy in COVID-19 to clarify the role of HDL in the pathogenesis of COVID-19 and discuss the potential of HDL therapy in COVID-19.
Highlights
Coronavirus disease 2019 (COVID-19), caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), outbroke in Wuhan in late 2019 (Guan W.-J. et al, 2020; Wang et al, 2020a; Huang C. et al, 2020; Hui et al, 2020; Lu et al, 2020)
A decline in total cholesterol, high-density lipoprotein (HDL), and low-density lipoprotein (LDL) levels in patients with COVID-19 has been observed in several studies, including our previous research (Wei et al, 2020a; Wang et al, 2020b)
Severe COVID-19 was associated with widespread activation of the coagulation system, corroborated by elevated activated partial thromboplastin time (APTT) and prothrombin time (PT) along with markedly elevated D-dimer levels (Tang et al, 2020; Zhou P. et al, 2020)
Summary
Coronavirus disease 2019 (COVID-19), caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), outbroke in Wuhan in late 2019 (Guan W.-J. et al, 2020; Wang et al, 2020a; Huang C. et al, 2020; Hui et al, 2020; Lu et al, 2020). It has since spread worldwide (Albarello et al, 2020; Giunta et al, 2020; Young et al, 2020). Abnormal coagulation function is a prominent feature in severe COVID-19 cases (Beltrán-García et al, 2020; José et al, 2020; Song et al, 2020; Zafer et al, 2021)
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