Latest research on Simvastatin

Simvastatin is a lipid-lowering agent that is derived synthetically from the fermentation of Aspergillus terreus. It is a potent competitive inhibitor of 3-hydroxy-3-methylglutaryl coenzyme A reductase (hydroxymethylglutaryl COA reductases), which is the rate-limiting enzyme in cholesterol biosynthesis. It may also interfere with steroid hormone production. Due to the induction of hepatic LDL receptors, it increases breakdown of LDL cholesterol. [PubChem]

Latest findings

The statin effects on EPC activity appear to be independent of the impact on LDL-C reduction, as shown by the comparison of Simvastatin with Ezetimibe administration [69], suggesting that the beneficial effect of lipid lowering drugs on the endothelium health status may be enhanced by EPC stimulation. [source, 2016]
The third published case of rhabdomyolysis was described 1 week post influenza vaccination in a 57 year old renal transplant patient on Simvastatin and Cyclosporin A [21]. [source, 2016]
Interestingly, cholesterol lowering-independent effects of plaque stabilization were observed with Simvastatin treatment [42]. [source, 2016]
However, a recent study of Simvastatin in patients with moderate to severe COPD without metabolic/cardiovascular indication for statins did not observe any reduction in COPD exacerbations. [source, 2016]
His regular medications included Irbesartan 150 mg once a day, Amlodipine 5 mg once a day, Simvastatin 20 mg once a day, alfacalcidol 0.25 microgram once a day and Sevelamer 800 mg three times a day with meals. [source, 2016]
Simvastatin administration 30 minutes before ischemia prevented the WIR-derived increment in intrahepatic vascular resistance, thus improving liver perfusion without changes in portal pressure (Fig. 4a). [source, 2016]
In addition, Simvastatin significantly attenuated the development of acute endothelial dysfunction both at 2 and 24 h of reperfusion as evidenced by improved vasodilation in response to Ach (Fig. 4b top) and reduced sinusoidal vWF expression (Fig. 4b bottom). [source, 2016]
Administration of Simvastatin prior to ischemia maintained liver KLF2 protein expression and eNOS phosphorylation levels, which was especially evident at 2 h of reperfusion (Fig. 5a). [source, 2016]
Liver endothelial phenotype maintenance due to Simvastatin administration prevented an increased expression in adhesion molecules (P-Selectin 55% lower at 2 h of reperfusion, and 98% at 24 h vs. vehicle-treated rats, p < 0.05; VCAM-1 Fig. 6), and neutrophil and macrophage infiltration (Fig. 6), both at the early and late phases of reperfusion. [source, 2016]
Simvastatin increased KLF2 mRNA expression not only in LSEC but also in primary hepatocytes and Kupffer cells (Supplementary Fig. S1a). [source, 2016]