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Background: Increased levels of inflammation markers in patients with kidney disease, particularly chronic kidney disease (CKD) is an important risk factor. This study explored whether the effect of more potent statins on inflammation in CKD patients is dose-dependent, whether there is any difference between the hydrophilic and lipophilic statins concerning their effects on inflammation markers in patients with CKD, and whether the duration of treatment with statins has any effect on markers of inflammation in these patients., Methods: A systematic literature search of Scopus, PubMed, and ISI Web of Science databases from inception to August 2022 was performed. Eligible studies were stratified based on a target population, intervention duration, dosage and type of statins (high intensity statin and moderate/ low intensity), and solubility of statins. Publication bias was evaluated using Begg's regression asymmetry test for visual inspection of funnel plots. Non-linear effects of dosage of statins and treatment duration were also examined by fractional polynomial modeling., Results: Meta-analysis of 10 RCTs (12 studies) on 264 patients with kidney disease and 254 controls showed a significant hs-CRP lowering effect of the dose of statin. Both hydrophilic and lipophilic statins had significant hs-CRP lowering effects. Meta-analysis of 6 publications (7 studies) evaluating the impact of statins on CRP in 235 patients and 197 control subjects showed a significant negative association between treatment with statins group and CRP levels., Conclusion: Statin treatment decreases significantly the levels of CRP and hs-CRP in patients with kidney disease., (Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.net.)

Statins are HMG-CoA reductase inhibitors and decrease plasma low-density lipoprotein cholesterol (LDL-C) levels. They are well tolerated, and because of their LDL-C-lowering effect, they are utilized to decrease the risk of atherosclerosis and cardiovascular disease. However, statins have pleiotropic effects, including immunomodulatory, anti-inflammatory, antioxidant, and anticancer. Currently, oral administration is the only Food and Drug Administration (FDA)-approved route of administration for statins. However, other administration routes have demonstrated promising results in different pre-clinical and clinical studies. For instance, statins also seem beneficial in dermatitis, psoriasis, vitiligo, hirsutism, uremic pruritus, and graft-versus-host disease. Topically applied statins have been studied to treat seborrhea, acne, rhinophyma, and rosacea. They also have beneficial effects in contact dermatitis and wound healing in animal studies, (HIV) infection, osseointegration, porokeratosis, and some ophthalmologic diseases. Topical and transdermal application of statins is a non-invasive drug administration method that has shown significant results in bypassing the first-pass metabolism in the liver, thereby reducing possible adverse effects. This study reviews the multifaceted molecular and cellular impacts of statins, their topical and transdermal application, novel delivery systems, such as nanosystems for topical and transdermal administration and the challenges concerning this approach., (Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.net.)

Heart failure (HF) is a public health issue that imposes high costs on healthcare systems. Despite the significant advances in therapies and prevention of HF, it remains a leading cause of morbidity and mortality worldwide. The current clinical diagnostic or prognostic biomarkers, as well as therapeutic strategies, have some limitations. Genetic and epigenetic factors have been identified to be central to the pathogenesis of HF. Therefore, they might provide promising novel diagnostic and therapeutic approaches for HF. Long non-coding RNAs (lncRNAs) belong to a group of RNAs that are produced by RNA polymerase II. These molecules play an important role in the functioning of different cell biological processes, such as transcription and regulation of gene expression. LncRNAs can affect different signaling pathways by targeting biological molecules or a variety of different cellular mechanisms. The alteration in their expression has been reported in different types of cardiovascular diseases, including HF, supporting the theory that they are important in the development and progression of heart diseases. Therefore, these molecules can be introduced as diagnostic, prognostic, and therapeutic biomarkers in HF. In this review, we summarize different lncRNAs as diagnostic, prognostic, and therapeutic biomarkers in HF. Moreover, we highlight various molecular mechanisms dysregulated by different lncRNAs in HF., (Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.net.)

One of the main causes of atherosclerosis is a disruption in cellular cholesterol hemostasis. The low-density lipoprotein receptor (LDLR) is an important factor in maintaining cholesterol homeostasis by the receptor-mediated endocytosis of LDL particles. Defective hepatic LDLR activity and uptake of LDL particles lead to elevated blood levels of low-density lipoprotein cholesterol (LDL-C), which is associated with a higher risk of atherosclerotic cardiovascular disease. LDLR expression can be affected by microRNAs (miRNAs). Some miRNAs, like miR-148a, miR-185, miR-224, miR-520, miR-128-1, miR-27a/b, miR-130b, and miR-301 seem to be important post-transcriptional regulators of LDLR related genes. These findings indicate the critical role of miRNAs in regulating LDL metabolism. The aim of this review was to provide insight into the miRNAs involved in LDLR activity and their potential roles in the treatment of cardiovascular disease., (Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.net.)

Resolvins are specialized pro-resolving mediators derived from omega-3 fatty acids that can suppress several cancer-related molecular pathways, including important activation of transcription parameters in the tumor cells and their microenvironment, inflammatory cell infiltration, cytokines as well as chemokines. Recently, an association between resolvins and an important anti-inflammatory process in apoptotic tumor cell clearance (efferocytosis) was shown. The inflammation status or the oncogene activation increases the risk of cancer development via triggering the transcriptional agents, including nuclear factor kappa-light-chain-enhancer of activated B cells by generating the pro-inflammatory lipid molecules and infiltrating the tumor cells along with the high level of pro-inflammatory signaling. These events can cause an inflammatory microenvironment. Resolvins might decrease the leukocyte influx into the inflamed tissues. It is widely accepted that resolvins prohibit the development of debris-triggered cancer via increasing the clearance of debris, especially by macrophage phagocytosis in tumors without any side effects. Resolvins D2, D1, and E1 might suppress tumor-growing inflammation by activation of macrophages clearance of cell debris in the tumor. Resolvin D5 can assist patients with pain during treatment. However, the effects of resolvins as anti-inflammatory mediators in cancers are not completely explained. Thus, based on the most recent studies, we tried to summarize the most recent knowledge on resolvins in cancers., (Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.net.)

Proprotein convertase subtilisin/Kexin type 9 (PCSK9) inhibitors are FDA-approved drugs recommended for high-risk patients with LDL-cholesterol (LDL-c) levels ≥ 70 mg/dl. Several studies have also investigated the relationship between PCSK9 and periodontitis. Specifically, studies have investigated the association between periodontitis and periodontal PCSK9 levels in humans, and periodontium status in PCSK9-knockout versus wild-type mice. While a positive association between periodontitis and periodontal PCSK9 levels has been noted, the findings on the comparison of periodontium status between PCSK9-knockout and wild-type mice have been inconsistent. Different methodologies among these studies may explain this discrepancy. Future experimental studies on the impact of pharmacological PCSK9 inhibition on periodontal status as well as observational studies comparing periodontium status between patients receiving PCSK9 inhibitors and those receiving other lipid-lowering drugs will shed light on the role of PCSK9 in periodontal health and disease., (Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.net.)

Background and Objectives: Some clinical trials have indicated the beneficial effects of statins in patients with kidney disease, while others have reported no positive effect of statins in these patients. We conducted this meta-analysis to identify the effects of statins on serum levels of interleukin-6 (IL-6) and Tumor Necrosis Factor Alpha (TNF-α) in patients with kidney disease., Designs and Methods: A systematic literature search was performed using PubMed, Scopus, and Web of Science databases to identify all studies published from inception to August, 2022. The major outcome variable was the Weighted Mean Difference (WMD). Eligible studies were stratified based on target population, intervention duration, dosage and type of statins, and solubility of statins., Results: Meta-analysis performed on seven publications (8 studies), including 213 patients with kidney disease and 188 control individuals, indicated that the concentration of IL-6 was marginally decreased in patients with kidney disease following statin therapy disease (WMD = -1.15 pg/mL; 95% CI = -2.33 to 0.04, P = 0.05, I 2 = 68.5%). The findings of subgroup analysis based on the dosage of statins showed that neither highintensity nor moderate/low-intensity statin treatment could significantly influence the serum level of IL-6. Lipophilic statins were more effective than hydrophilic statins, and they marginally decreased the levels of IL-6 (WMD = -1.21 pg/mL; 95% CI = -2.43 to 0, P = 0.05, I2 = 55.7%). Meta-analysis of four publications (five studies) with 157 patients with kidney disease and 132 control subjects showed that statins reduced the serum levels of TNF-α in patients with kidney disease when compared with control individuals (WMD= -2.66 pg/mL; 95% CI = -4.26 to -1.06, P < 0.001, I 2 = 63%)., Conclusion: Statins only marginally decreased the concentration of IL-6 in patients with kidney disease, but neither high-intensity nor moderate/low-intensity statin treatment could significantly influence the level of IL-6. However, statins reduced serum levels of TNF-α in patients with kidney disease., (Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.net.)

Background: Gut microbiota is associated with an increased risk of atherosclerotic cardiovascular disease (ASCVD) through the metabolites, which can induce atherogenesis. One of these metabolites is trimethylamine N-oxide (TMAO). Some studies indicate that statins do not only decrease LDL-cholesterol and thus ASCVD risk, but they also affect gut microbiota. There are only a few studies on humans suggesting that statins might also decrease TMAO, but their results are not unanimous. This meta-analysis aimed to provide an answer as to whether statins do affect decreasing the plasma levels of atherogenic TMAO., Methods: A systematic literature search in PubMed, Scopus, Embase, and Web of Science was performed from inception to January 1st, 2023. To assess the quality of each study included in the meta-analysis, the Cochrane Quality Assessment tool 1 (ROB 1) was used. Comprehensive Meta-Analysis V3 software was used to perform the meta-analysis. The weighted mean difference was also used. A random effects meta-analysis was used to calculate the overall estimate of effect size. In the leave-one-out approach, one study was excluded from each analysis to evaluate the effect of each study on the overall effect size., Results: Random-effects meta-analysis of 3 studies including 244 patients demonstrated a significant decrease in plasma TMAO levels after statin treatment (WMD: -1.839, 95% CI: -2.391, -1.287, p<0.001; I2 :0). The reduction in TMAO was robust in the leaveone-out sensitivity analysis., Conclusion: Statins might reduce TMAO levels, but there is a need for further evidence from long-term studies taking into account different types and doses of statins., (Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.net.)

Background: Statins are the main lipid-lowering drugs and are used in the prevention of cardiovascular diseases (CVDs). Since the results have been, to some extent, inconsistent in the clinical trials concerning different types of CVDs, a systematic review and meta-analysis was performed to prove the effect of statins on decreasing elevated levels of total cholesterol, triglycerides (TG), low-density lipoprotein cholesterol (LDL-C), and high-density lipoprotein cholesterol (HDL-C) in patients with CVDs., Methods: Literature search was performed on major electronic databases (MEDLINE/ PubMed, Scopus, and ISI Web of Science) from inception up to July 2021 to find randomized controlled trials (RCTs) evaluating the effect of different statins on different types of CVDs. The effect size was determined using weighted mean difference (WMD) and corresponding 95% confidence interval (CI)., Results: Statin therapy significantly decreased levels of total cholesterol (WMD = -33.37 mg/dl, 95% CI: -45.98 to -20.76, P<0.001), LDL-C (WMD = -29.42 mg/dl, 95% CI: -36.81 to -22.03, P<0.001), and TG (WMD = -15.19 mg/dl, 95% CI = -26.41 to -3.97, P<0.001), and increased levels of HDL-C (WMD = 1.55 mg/dl, 95% CI: 0.20, to 2.90, P=0.02) in patients with different CVDs., Conclusion: Statin therapy was found effective in lowering levels of total cholesterol, LDL-C, and TG, and increasing levels of HDL-C in patients with different CVDs., (Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.net.)

Background: One of the major indications for digoxin use is the treatment of heart failure (HF). Although the clinical application of digoxin in long-term outcomes in patients with HF and reduced ejection fraction (HFrEF) patients is well explained, the association between digoxin therapy and outcomes in patients with HF and preserved ejection fraction (HFpEF) is not very clear., Objectives: The aim of this study was to show the clinical efficacy of digoxin on long-term outcomes in subjects with HFpEF., Methods: PubMed, Embase, Scopus and Web of Science (ISI) electronic databases were searched until May 2021 to obtain relevant studies. The primary outcome was all-cause mortality attributed to treatment with digoxin. The secondary outcomes were "all-cause hospitalization", "hospitalization because of HF" and "all-cause mortality or hospitalization of HF"., Results: Seven studies with more than 23000 patients with HFpEF, of which more than 4900 were treated with digoxin, fulfilled the eligibility criteria and were included in this meta-analysis. Treatment with digoxin was associated with a neutral effect on all-cause mortality (HR 1.04, 95 % CI 0.91-1.20, I2 = 57.9 %), all-cause hospitalization (HR 0.97, 95 % CI 0.88-1.07, I2 = 0.0 %), HFhospitalization (HR 0.96, 95 % CI 0.90-1.02, I2 = 41.4 %), and all-cause mortality or HFhospitalization (HR 1.07, 95 % CI 0.91-1.26, I2 = 81.2 %). In subgroup meta-analyses based on ejection fraction (EF), treatment with digoxin did not significantly alter these outcomes in each subset of patients., Conclusion: The results of this meta-analysis suggest that digoxin does not have any significant effect on long-term outcomes of HFpEF patients, including "all-cause mortality", "all-cause hospitalization", "hospitalization because of HF" and "all-cause mortality or hospitalization of HF"., (Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.net.)

Objective: To evaluate the effectiveness of the Partnership Care Model (PCM) on health-related quality of life (HRQoL) in adults with chronic diseases. Methods Data Sources/Study Setting: Existing literature dealing with the effect of HRQoL on chronic patients according to the HRQoL outcomes based on SF36 questionnaires., Study Design: Systematic review and meta-analysis., Data Collection: Medline, PubMed, Scopus, Web of Science, Embase, Cochran database and Persian databases, including SID, Magiran, Iranmedex, and Irandoc, were searched according to the MeSH terms until May 15, 2022. Data analysis was made by using the random effects model and heterogeneity by I 2 index, and all analyses were made by STATA vers.16 (Stata Corp, College Station, Texas, USA)., Principal Findings: Three studies were included in the meta-analysis. Computing the common effect size, there was a significant intervention effect in all HRQoL dimensions, physical and mental subscales, as well as HRQoL total score. The results showed that there was significantly moderate to high substantial heterogeneity between studies except for vitality (I 2 =45.9%, P=0.157) and physical functioning (I 2 =30.9%, P=0.235) dimensions., Conclusion: According to the results of the study and realizing the efficiency of PCM on the eight dimensions of quality of life of chronic patients, it can be stated that this national model, which is in line with the culture and context of Iran, is effective, simple, efficient and reliable. It can be used in the promotion and improvement of various dimensions of HRQoL in chronic diseases., (Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.net.)

Cardiovascular diseases are some of the major causes of morbidity and mortality in developed and developing countries. Cardiac fibrosis is one of the most often pathological changes of heart tissues. It occurs as a result of extracellular matrix proteins accumulation at myocardia. Cardiac fibrosis results in impaired cardiac systolic and diastolic functions and is associated with other effects. Therapies with medicines have not been sufficiently successful in treating chronic diseases such as CVD. Therefore, the interest for therapeutic potential of natural compounds and medicinal plants has increased. Plants such as grapes, berries and peanuts contain a polyphenolic compound called "resveratrol" which has been reported to have various therapeutic properties for a variety of diseases. Studies on laboratory models show that resveratrol has beneficial effects on cardiovascular diseases, including myocardial infarction, high blood pressure cardiomyopathy, thrombosis, cardiac fibrosis, and atherosclerosis. In vitro animal models using resveratrol indicated protective effects on the heart by neutralizing reactive oxygen species, preventing inflammation, increasing neoangiogenesis, dilating blood vessels, suppressing apoptosis and delaying atherosclerosis. In this review, we are presenting experimental and clinical results of studies concerning resveratrol effects on cardiac fibrosis as a CVD outcome in humans., (Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.net.)

Familial hypercholesterolemia (FH) as a high-frequency genetic disorder is diagnosed based on family and/or patient's history of coronary heart disease (CHD) or some other atherosclerotic diseases, LDL-C levels, and/or clinical signs such as tendinous xanthoma, arcus cornealis before age 45 years as well as a functional mutation in the LDLR, apoB or PCSK9 gene. Its clinical features are detectable since early childhood. Early diagnosis and timely treatment increase life expectancy in most patients with FH. Current FH therapies decrease the level of lowdensity lipoprotein up to ≥50% from baseline with diet, pharmacotherapeutic treatment, lipid apheresis, and liver transplantation. The cornerstone of medical therapy is the use of more potent statins in higher doses, to which often ezetimibe has to be added, but some FH patients do not achieve the target LDL-C with this therapy Therefore, besides these and the most recent but already established therapeutic approaches including PCSK9 inhibitors, inclisiran, and bempedoic acid, new therapies are on the horizon such as gene therapy, CRISPR/Cas9 strategy, etc. This paper focuses on cellular and molecular potential strategies for the treatment of FH., (Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.net.)

The inverse relationship between low plasma high-density lipoprotein cholesterol (HDL-C) concentrations and increased risk of Atherosclerotic Cardiovascular Disease (ASCVD) is well-known. However, plasma HDL-C concentrations are highly variable in subjects with ASCVD. In clinical outcome trials, pharmacotherapies that increase HDL-C concentrations are not associated with a reduction in ASCVD events. A causal relationship between HDL-C and ASCVD has also been questioned by Mendelian randomization studies and genome-wide association studies of genetic variants associated with plasma HDL-C concentrations. The U-shaped association between plasma HDL-C concentrations and mortality observed in several epidemiological studies implicates both low and very high plasma HDL-C concentrations in the etiology of ASCVD and non- ASCVD mortality. These data do not collectively support a causal association between HDL-C and ASCVD risk. Therefore, the hypothesis concerning the association between HDL and ASCVD has shifted from focus on plasma concentrations to the concept of functionality, in particular cellular cholesterol efflux and HDL holoparticle transport. In this review, we focus on these new concepts and provide a new framework for understanding and testing the role of HDL in ASCVD., (Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.net.)

Background: The findings of trials investigating the effects of L-carnitine administration on serum lipids are inconsistent. This meta-analysis of randomized controlled trials (RCTs) was performed to summarize the effects of L-carnitine intake on serum lipids in patients and healthy individuals., Methods: Two authors independently searched electronic databases including MEDLINE, EMBASE, Cochrane Library, Web of Science, PubMed and Google Scholar from 1990 until August 1, 2019, in order to find relevant RCTs. The quality of selected RCTs was evaluated using the Cochrane Collaboration risk of bias tool. Cochrane's Q test and I-square (I2) statistic were used to determine the heterogeneity across included trials. Weight mean difference (SMD) and 95% CI between the two intervention groups were used to determine pooled effect sizes. Subgroup analyses were performed to evaluate the source of heterogeneity based on suspected variables such as, participant's health conditions, age, dosage of L-carnitine, duration of study, sample size, and study location between primary RCTs., Results: Out of 3460 potential papers selected based on keywords search, 67 studies met the inclusion criteria and were eligible for the meta-analysis. The pooled results indicated that L-carnitine administration led to a significant decrease in triglycerides (WMD: -10.35; 95% CI: -16.43, -4.27), total cholesterol (WMD: -9.47; 95% CI: - 13.23, -5.70) and LDL-cholesterol (LDL-C) concentrations (WMD: -6.25; 95% CI: -9.30, -3.21), and a significant increase in HDL-cholesterol (HDL-C) levels (WMD: 1.39; 95% CI: 0.21, 2.57). L-carnitine supplementation did not influence VLDL-cholesterol concentrations. When we stratified studies for the predefined factors such as dosage, and age, no significant effects of the intervention on triglycerides, LDL-C, and HDL-C levels were found., Conclusion: This meta-analysis demonstrated that L-carnitine administration significantly reduced triglycerides, total cholesterol and LDL-cholesterol levels, and significantly increased HDL-cholesterol levels in the pooled analyses, but did not affect VLDL-cholesterol levels; however, these findings were not confirmed in our subgroup analyses by participant's health conditions, age, dosage of L-carnitine, duration of study, sample size, and study location., (Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.net.)

Background: Atherosclerosis is a chronic inflammatory disease and a leading cause of coronary artery disease, peripheral vascular disease and stroke. Lipid-laden macrophages are derived from circulating monocytes and form fatty streaks as the first step of atherogenesis., Methods: An electronic search in major databases was performed to review new therapeutic opportunities for influencing the inflammatory component of atherosclerosis based on monocytes/macrophages targeting., Results: In the past two decades, macrophages have been recognized as the main players in atherogenesis but also in its thrombotic complications. There is a growing interest in immunometabolism and recent studies on metabolism of macrophages have created new therapeutic options to treat atherosclerosis. Targeting recruitment, polarization, cytokine profile extracellular matrix remodeling, cholesterol metabolism, oxidative stress, inflammatory activity and non-coding RNAs of monocyte/macrophage have been proposed as potential therapeutic approaches against atherosclerosis., Conclusion: Monocytes/macrophages have a crucial role in progression and pathogenesis of atherosclerosis. Therefore, targeting monocyte/macrophage therapy in order to achieve anti-inflammatory effects might be a good option for prevention of atherosclerosis., (Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.net.)

Background: Plasma homocysteine is an independent non-traditional risk factor for atherosclerotic cardiovascular disease. The impact of statin therapy on plasma homocysteine is not conclusive., Objective: To evaluate the effect of statin therapy on plasma homocysteine concentrations in a systematic review and meta-analysis of controlled clinical trials. The secondary aim was to assess the comparative effect of statins versus fibrates on plasma homocysteine levels in head-to-head trials., Method: PubMed-Medline, SCOPUS, Web of Science and Google Scholar databases were searched (from the first reports to March 07, 2016) to identify controlled trials evaluating the impact of statins on plasma homocysteine concentrations. A systematic assessment of bias in the included studies was performed using the Cochrane criteria. A random-effects model and generic inverse variance method were used for quantitative data synthesis. Sensitivity analysis was conducted using the leave-one-out method. Random-effects meta-regression was performed using unrestricted maximum likelihood method to evaluate the impact of potential moderators., Results: Meta-analysis of data from 7 studies did not suggest a significant alteration in plasma homocysteine concentrations following treatment with statins compared with the control group (WMD: -0.59 μmol/L, 95% CI: -1.66, 0.48, p=0.279; I2=52.53%). However, meta-analysis of 9 studies suggested a significantly greater reduction of plasma homocysteine concentrations with statins compared with fenofibrate (WMD: -4.81 μmol/L, 95% CI: -5.39, -4.23, p<0.001; I2=0%). Results of both analyses were robust in the sensitivity analysis., Conclusion: Statin therapy is not associated with a significant alteration of plasma homocysteine levels, while fenofibrate increases the homocysteine levels when compared with statins.

Statins reduce cardiovascular mortality and morbidity as well as cardiovascular events in patients with a very high risk of cardiovascular disease (CVD) and also in subjects with high or moderate risk by reducing the levels of low-density lipoprotein cholesterol (LDL-C). Although they are considered to be drugs with a very good safety profile, because of their wide use there are many concerns that their adverse effects might compromise their proven beneficial effects. Therefore this article reviews all the data and provides an evidence- based insight what are the proven adverse effects of statins and what are the "myths" about them. The most important side effects include myopathy and rhabdomyolysis. Another side effect is increased activity of liver tests which occurs occasionally and is reversible. However, recent studies even suggest that statin therapy can improve hepatic steatosis. It is beyond any doubt that statins do slightly increase the incidence of type 2 diabetes mellitus in people with two or more components of metabolic syndrome but the cardiovascular benefits of such a treatment by far exceed this risk. Statin therapy has also been associated with some adverse renal effects, eg. acute renal failure, but recent data suggest even a possible protective effect of these drugs on renal dysfunction. Concerns that statins might increase cancer have not been proven. On the contrary, several studies have indicated a possible benefit of these drugs in patients with different types of cancer. Early concerns about cognitive dysfunction and memory loss associated with statins use could not be proven and most recent data even suggest a possible beneficial effect of statins in the prevention of dementia. Systematic reviews and clinical guidelines suggest that the cardiovascular benefits of statins by far out-weight non-cardiovascular harms in patients with cardiovascular risk.