PROS | ||
AREA OF INTEREST | Action of statins | CLINICAL EFFECTS IN PATIENTS COVID-19 |
Immunomodulation [10] | Stabilization of MyD88 levels during hypoxia and stress, mitigating the action of NF-kB | Potential to reduce the severity of SARS-CoV2 infection |
Inflammation [13] [14] | 1) Reduction of LDL cholesterol levels, thereby reducing direct LDL cholesterol mediated inflammation 2) Inhibition of prenylation of G proteins, leading to down-regulation of NF-kB, suppression of pro-inflammatory cytokines (TNF a, IL-6) and chemokines (IL-8) | Potential role in reduction of SARS-CoV2 induced lung injury and protection from cytokine storm |
Oxidative Stress [18] | Reduction of oxidative injury/maintenance of the redox balance of the endothelium by: 1) Upregulation of nitric oxide syntliase 2) Suppression of pro-oxidant enzymes (NADPH oxidase) | Potential role in reduction of SARS-CoV2 induced lung injury |
Thrombosis [21] [22] | 1. Anti-platelet effect (Lipid dependent and lipid independent mechanisms) 2. Weak anti-thrombotic effect 1) Prevents the conversion of factor X to Xa by down regulating tissue factor 2) Uoregulation of thrombomodulin to bind thrombin | Potential to reduce/prevent venous and arterial thrombus formation |
Membrane (lipid) rafts [23] | Disruption of lipid rafts by depletion of cholesterol from the plasma membrane, which might alter the assembly of angiotensin converting enzyme 2 receptors (act as co-receptors for SARS-CoV2 entry into the cell) | Theoretical possibility ofreducing viral entry, leading to low viral titres and infectivity |
(ACE2) [4] [24] | Upregulation of expression of ACE2 | Potential to reduce SARS-CoV2 induced lung injury mediated by excess Angiotensin-11 |
SARS-CoV2 main protease [26] | Efficient inhibitors of SARS-CoV2 main protease (Computational molecular docking method) | Potential to directly inhibit the virus, reducing viral load |
CONS | ||
Tot cholesterol/ LDL cholesterol levels [7] | Reduction of serum total and LDL cholesterol | Speculated that this might increase morbidity/mortality from SARS-CoV2 infection, as elevated illL cholesterol is protective since illL particles adhere to and inactivate microorganisms and their toxins |
Immunomodul ation [10] | Inhibition of MyD88 expression | Speculated to reduce innate immunity response, thereby worsening infection |
Angiotensin converting enzyme 2 (ACE2) [24] | Upregulation of expression of ACE2 | Potential to increase SARS-CoV2 entry into cells |
Myositis and liver dysfunction [31] [32] [33] [34] | I. Mild elevation of liver enzymes in 10%, and elevation >3 times upper limit of normal in 1% - 3% 2. Myalgia in 2% - 7% | Detrimental effect in people with COVID-19 with skeletal muscle symptoms or liver dysfunction |
Drug interactions [35] [37] | Inhibition of cytochrome P-450 group of enzymes by protease inhibitors used in COVID-19 may significantly increase statin levels | Increased risk of toxicity: myopathy and rhabdomyolysis |