Latest research on Rosuvastatin

Rosuvastatin is an antilipemic agent that competitively inhibits hydroxymethylglutaryl-coenzyme A (HMG-CoA) reductase. HMG-CoA reducuase catalyzes the conversion of HMG-CoA to mevalonic acid, the rate-limiting step in cholesterol biosynthesis. Rosuvastatin belongs to a class of medications called statins and is used to reduce plasma cholesterol levels and prevent cardiovascular disease.

Rosuvastatin side effects

Hyperlipidemic patients administered with Rosuvastatin 10 or 20 mg/day for 3 months, for example, show a dose-dependent increase in urinary low-molecular protein α-1 microglobulin 176. [source, 2015]
Such reduction in carotid intima media thickness was comparable to or greater than the effects observed from some statins: pitavastatin decreased carotid intima media thickness by 0.024 mm/year in patients with known atherosclerosis,[46] while Rosuvastatin decreased carotid intima media thickness by 0.0014 mm/year among low-risk individuals. [source, 2015]
These findings complement and extend the above-mentioned meta-analyses [24] as well as the results from the Justification for the Use of Statins in Primary Prevention: An Intervention Trial Evaluating Rosuvastatin (JUPITER) trial [27], which reported that statins reduced death from any cause by 12 %. [source, 2016]
This was associated with the idea that Rosuvastatin increased Akt, ERK phosphorylation, promoted the subsequent FoxO3a phosphorylation and nuclear export, and decreased the proapoptotic proteins in ADSCs [119]. [source, 2016]
Rosuvastatin administration reduced AAA progression in the Ang II model, and increased HO enzyme activity, independent of changes in lipid profile. [source, 2016]
On the contrary, Rosuvastatin did not affect baseline leukocytes' count or the postprandial neutrophils' increase in CAD patients [44]. [source, 2016]
In a BDL model performed in rats, the administration of Rosuvastatin in early stages of cholestasis decreased α-SMA expression and inhibited NF-κB activation but also increased hepatocytolysis, oxidative stress formation, and hepatic inflammation and sustained increased levels of TGF-β1 (Olteanu et al., 2012). [source, 2016]
In brief, Rosuvastatin was associated with a 44% (hazard ratio [HR], 0.56; 95% confidence interval [CI], 0.46–0.69; P<0.00001) reduction in the trial primary end point, a composite of nonfatal MI, nonfatal stroke, hospitalization for unstable angina, arterial revascularization, or death resulting from cardiovascular causes. [source, 2015]
Atorvastatin (Lipitor), mevastatin (Compactin) and rosuvastatin (Crestor) increased basal PAI-1-Luc activity 2.5-3-fold in cultured cells (Fig 1A). [source, 2015]
Due to a family history of myocardial infarction and a low-density lipoprotein (LDL) cholesterol level of 1.62 g/L, Atorvastatin was prescribed at a dose of 10 mg/day in November 2011 but caused severe myalgia and was rapidly replaced by Rosuvastatin at a dose of 5 mg/day. [source, 2015]