Question: What do statins do?

Context:
Statins are inhibitors of HMG-CoA reductase, the enzyme that catalyzes the reduction of HMG-CoA to mevalonic acid by NADPH
Statins, which specifically inhibit HMG Co-A reductase, the rate-limiting step of cholesterol biosynthesis, are widely prescribed to reduce serum cholesterol and cardiac risk,
OBJECTIVES: Statins are a lipid-lowering treatment, prescribed frequently to prevent cardiovascular events.
The doctors' beliefs about statins' ability to prolong life were associated significantly with their willingness to initiate treatment.CONCLUSION: The overall results imply that doctors have varying and suboptimal understanding of the effect of statins.
However, the meta-regression analysis indicated that age of study participants modified the association between statin use and cancer risk (P = .003).CONCLUSION: Our findings do not support a protective effect of statins against cancer.
What is less well known is a phenomenon whereby statins may induce a myopathy, which persists or may progress after stopping the drug.
Statins can cause a necrotizing myopathy and hyperCKaemia which is reversible on cessation of the drug.
* Our data do not show any beneficial effect of statins in reducing disease inflammation in RA patients.AIM: To investigate the possible anti-inflammatory effect of statins in a cohort of rheumatoid arthritis (RA) patients.METHODS: We conducted a cohort study consisting of all patients with at least one claim for RA using LifeLink, a health insurance claims database.
Statins are widely used in kidney transplant patients given their established benefits in the general population, however evidence favouring their use is lacking.To assess the benefits and harms of statin therapy on mortality and renal outcomes in kidney transplant recipients.We searched MEDLINE, EMBASE, the Cochrane Central Register of Controlled Trials (CENTRAL), and hand searched reference lists of articles and scientific proceedings.Randomised controlled trials (RCTs) and quasi-RCTs comparing statins with placebo, no treatment or other statins in kidney transplant recipients.Two authors independently assessed study quality and extracted data
Thus, it is important to understand whether other signaling pathways that are involved in atherosclerosis could be targets of statins, and if so, whether individuals with "overactivity" of these pathways could benefit from statin therapy, regardless of serum cholesterol level.Statins inhibit the synthesis of isoprenoids, which are important for the function of the Rho/Rho-associated coiled-coil containing kinase (ROCK) pathway
Evidence for statins in people who have had a kidney transplant were sparse and lower quality due to imprecise effect estimates and provided limited systematic evaluation of treatment harm.Statins may reduce cardiovascular events in kidney transplant recipients, although treatment effects are imprecise
Statins decreased 24-hour urinary protein excretion (6 studies, 311 patients: MD -0.73 g/24 h, 95% CI -0.95 to -0.52), but there was no significant improvement in creatinine clearance - a surrogate marker of renal function (11 studies, 548 patients: MD 1.48 mL/min, 95% CI -2.32 to 5.28).The incidence of rhabdomyolysis, elevated liver enzymes and withdrawal rates due to adverse events (well known complications of statins use), were not significantly different between patients receiving statins and placebo.Statins significantly reduced the risk of all-cause and cardiovascular mortality in CKD patients who are not receiving renal replacement therapy.
Statins are less cost-effective when obtained at average retail prices, particularly in patients at lower CVD risk.Although statins reduce absolute CVD risk in patients with CKD, the increased risk of rhabdomyolysis, and competing risks associated with progressive CKD, partly offset these gains
In this review, we debate the relative effect of statins in driving insulin resistance and the impairment of insulin secretion.Narrative overview of the literature synthesizing the findings of literature was retrieved from searches of computerized databases, hand searches, and authoritative texts employing the key words "Statins", "Randomized Clinical Trial", "Insulin sensitivity", "Insulin resistance", "Insulin Secretion", "Diabetes Mellitus" alone and/or in combination.The weight of clinical evidence suggests a worsening effect of statins on insulin resistance and secretion, anyway basic science studies did not find a clear molecular explanation, providing conflicting evidence regarding both the beneficial and the adverse effects of statin therapy on insulin sensitivity.
This study was undertaken to investigate the immunomodulatory mechanisms of statins that target the IFN response in PDCs.We isolated human blood PDCs by flow cytometry and examined the effects of simvastatin and pitavastatin on PDC activation, IFNalpha production, and intracellular signaling.Statins inhibited IFNalpha production profoundly and tumor necrosis factor alpha production modestly in human PDCs in response to Toll-like receptor ligands
The earlier JUPITER (Justification for the Use of Statins in Primary Prevention) trial provided appealing evidence that the risk of venous thrombosis may be lowered by statins
Statins (HMG-CoA reductase inhibitors) decrease postoperative adhesions by increasing peritoneal fibrinolytic activity.
Statins (HMG-CoA reductase inhibitors) reduce CD40 expression in human vascular cells.
HMG-CoA reductase inhibitors (statins) activate expression of PPARalpha/PPARgamma and ABCA1 in cultured gallbladder epithelial cells.
HMG-CoA reductase inhibitors (statins) might cause high elevations of creatine phosphokinase (CK) in patients with unnoticed hypothyroidism.
HMG-CoA reductase inhibitors (statins) reduce hypertrophic scar formation in a rabbit ear wounding model.
HMG-CoA reductase inhibitors, statins, induce phosphorylation of Mdm2 and attenuate the p53 response to DNA damage.
The target for statins, HMG-CoA reductase, is expressed in ductal carcinoma-in situ and may predict patient response to radiotherapy.
Two meta-analyses have shown statins do not improve survival, whereas two others showed improved cardiac function and reduced inflammation in HF. It appears lipophilic statins produce better survival and other outcome benefits compared to hydrophilic statins.
Statins are the current basis of lipid-lowering therapy, despite which may have limitations on efficacy and safety. In high risk patients who do not achieve current lipid goals, in those intolerant to statins or those with atherogenic dyslipidemia, it is possible combine two or more lipid lowering drugs, including statins, ezetimibe, bile acid sequestrants, fibrates, niacin and prescription omega-3 fatty acids.
Statins are the current basis of lipid-lowering therapy, despite which may have limitations on efficacy and safety. In high risk patients who do not achieve current lipid goals, in those intolerant to statins or those with atherogenic dyslipidemia, it is possible combine two or more lipid lowering drugs, including statins, ezetimibe, bile acid sequestrants, fibrates, niacin and prescription omega-3 fatty acids. However, for most of these combination therapies pivotal data on clinical outcomes are still lacking.
Statins are the current basis of lipid-lowering therapy, despite which may have limitations on efficacy and safety.
However, the findings of two large RCTs do not support the evidence provided by previous studies and suggest statins lack beneficial effects in HF.
Subsequently, a number of nonrandomised studies have shown statins improve clinical outcomes in patients with heart failure (HF).
AND WHAT DOES THE STUDY ADD?: Statins have shown broad spectrum anti-cancer properties in laboratory studies.
Statin-induced myopathy is an important cause of statin intolerance and the most common cause of statin discontinuation.
These findings underscore the need to better define the pathophysiology of statin-induced myalgia and develop methodologies to guide treatment of statin-intolerant patients..

Answer: Statins lower high cholesterol
Statins, which specifically inhibit HMG Co-A reductase, the rate-limiting step of cholesterol biosynthesis, are widely prescribed to reduce serum cholesterol and cardiac risk,