Statins, cholesterol and atherosclerosis

Production of cholesterol in the liver starts from conversion of Acetyl CoA to HMG CoA molecule.
HMG CoA is then converted by HMG CoA reductase enzyme into Mevalonate.
which after series of reactions transformed into Farnesyl PP molecule which then produce cholesterol
The newly produced cholesterol molecules in the liver are transported to very low-density lipoproteins abbreviated as VLDL
which deliver them to various extrahepatic destinations
In the blood VLDL is converted into low density lipoproteins abbreviated as LDL.
LDL also known as the bad cholesterol.
Why?
Because they are precipitated in the vascular walls and contribute the plaque formation or atherosclerosis
HMG CoA reductase inhibitors known as statins are group of drugs that have similar structure to HMG CoA molecule.
Therefore, they competitively inhibit the activity of HMG CoA reductase enzyme.
As a result, the production line of cholesterol production is largely interrupted
Reduced intrahepatic cholesterol production means there are less cholesterol will be transported into VLDL and less bad LDL molecules will be formed in the circulation.
And that is good.
Because less LDL will be precipitated in the vascular walls.
So statins drugs enhance plaque stabilization.
Additionally, reduced intrahepatic cholesterol production promotes DNA production of more LDL receptors.
These receptors are transported into the hepatocytes cell membrane…….where they LDL molecules are attracted to them.
The LDL- LDL receptor complexes are then endocytosed into the hepatocytes’ cytoplasm away from the circulation.
Thus, statins significantly reduce LDL levels in the circulations.
Finally, the intermediate molecule Farnesyl PP contribute to production of what’s known as Prenylated proteins.
Inhibition of HMG CoA reductase enzymes by statins will decrease farnesyl PP and the prenylated proteins.
This inhibition of prenylated proteins results in some positive effects such as improve endothelial functions.