Bridging the gap between CVD and COVID-19: the oxidized LDL hypothesis

Area of Science:

• Cardiovascular Medicine
• Virology
• Biochemistry

Background:

• Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) causes COVID-19, impacting cardiovascular health.
• Endothelial dysfunction (ED), linked to cardiovascular disease (CVD), plays a key role in COVID-19 pathogenesis.
• COVID-19-associated ED may stem from dysregulated lipid metabolism, with low high-density lipoprotein (HDL) correlating with disease severity.

Purpose of the Study:

• To hypothesize that targeting inflammatory dyslipidemia can benefit COVID-19 patients.
• To explore the link between lipid metabolism, endothelial dysfunction, and COVID-19 complications.
• To investigate the role of myeloperoxidase oxidized low-density lipoprotein (Mox-LDL) in COVID-19 pathogenesis.

Main Methods:

• Review of emerging evidence on COVID-19, CVD, and lipid metabolism.
• Analysis of the role of angiotensin-converting enzyme 2 (ACE 2) in viral entry and cardiovascular symptoms.
• Examination of the anti-fibrinolytic activity of Mox-LDL in endothelial cells.

Main Results:

• ACE 2 expression on endothelium may explain cardiovascular symptoms in COVID-19.
• Impaired HDL antioxidant capacity can lead to oxidized LDL (oxLDL) and Mox-LDL generation.
• Mox-LDL exhibits anti-fibrinolytic activity, potentially increasing risks of disseminated intravascular coagulation and ischemic strokes.

Conclusions:

• Inflammatory dyslipidemia is a significant factor in COVID-19 pathogenesis.
• Targeting inflammatory dyslipidemia presents a promising therapeutic strategy for COVID-19.
• Further research into lipid metabolism modulation could improve clinical outcomes for COVID-19 patients.