Statins are HMG-CoA reductase inhibitors, thereby reducing cholesterol synthesis, and thus were known early on as a lipid-lowering agent. Statins are hydroxymethylglutaryl coenzyme A (HMG-CoA) reductase inhibitors that block the intracellular hydroxymethylglutaric acid metabolic pathway by competitively inhibiting the endogenous cholesterol synthesis rate-limiting enzyme (HMG-CoA) reductase, resulting in a decrease in intracellular cholesterol synthesis, and thus feedback stimulation of the number and activity of low density lipoprotein (LDL) receptors on the cell membrane surface (mainly in hepatocytes). The number and activity of low density lipoprotein (LDL) receptors on the cell membrane surface (mainly in hepatocytes) are increased, resulting in increased clearance and lower levels of serum cholesterol. Statins also inhibit hepatic synthesis of apolipoprotein B-100, thereby reducing the synthesis and secretion of triglyceride-rich AV and lipoproteins. Statins have had great success since the first statin was introduced in 1973. Since the introduction of the first statin, mevastatin, in 1976, a growing family of statins has now been established. Statins are divided into natural compounds (e.g. lovastatin, simvastatin, pravastatin, mevastatin) and fully synthetic compounds (e.g. fluvastatin, atorvastatin, cerivastatin (withdrawn from the market), rasulvastatin, pitavastatin) are the most classical and effective lipid-lowering drugs, which are widely used in the treatment of hyperlipidemia. In addition to their lipid-regulating effects, statins can inhibit the inflammatory response of vascular endothelium, stabilize atheromatous plaques and improve vascular endothelial function when applied early in acute patients with acute coronary syndrome. Delaying the degree of atherosclerosis (AS), anti-inflammatory, neuroprotective and antithrombotic effects. The 4S study in 1994 was the first to clarify that simvastatin lipid-modifying therapy could significantly reduce mortality in patients with dyslipidemia by up to 30% while lowering LDL-C, and simultaneously reduce the occurrence of heart attacks and the need for coronary revascularization. Since then, studies on statin therapy to improve patient prognosis have emerged in succession. Recent studies have shown that statins have a protective effect on the kidney by reducing urinary protein and slowing the progression of renal atherosclerosis. This effect is associated with inhibition of tethered cell proliferation, inhibition of inflammatory factor expression and reduction of extracellular matrix deposition, in addition to indirect benefits through lipid lowering. In addition, several large pharmacological clinical studies have shown that statins help to improve renal function in patients with atherosclerosis. The Greek Atorvastatin and Coronary Heart Disease Evaluation Study (GREACEStudy) found that an average daily dose of 24 mg of atorvastatin reduced overall coronary heart disease mortality and coronary events in 1,600 Greek patients with coronary heart disease. The study’s showed that long-term active statin therapy significantly improved kidney function. Among 704 patients not receiving statins, creatinine clearance increased by 4.9% in the “usual” treatment group and by 12% in the intensive treatment group with atorvastatin. In the Heart Protection Study (HP S), all patients had decreased renal function after 4.6 years of follow-up, but this trend was significantly slowed by simvastatin. In addition to lipid-lowering and cardioprotective effects, statins have been suggested to have antiproliferative, anti-inflammatory, microthrombotic, and endothelial NO expression-inducing effects, and statin therapy can reverse pulmonary hypertension and has applications in heart failure, antiarrhythmia, tumor control, sepsis control, autoimmune diseases, and Alzheimer’s disease treatment. The first statin (Mevastatin, mevastatin) was discovered by Japanese pharmacologist Akira Endo in 1973, but the drug was so toxic that it eventually could not be introduced and is now a raw material for the production of pravastatin. The first company to successfully develop and market statins was Merck Sharp & Dohme, whose product lovastatin is still widely used today. It can be argued that statins are the most successful new clinical drug class ever developed in the United States, with the best sales and few major setbacks. Therefore, major companies including Merck, Pfizer, Schering-Plough, Novartis, Bristol-Myers Squibb and AstraZeneca have statin lines. The only one that suffered a setback was Bayer’s cerivastatin, trade name: “Bystein”. The Baystatin Incident In 1997, Bayer of Germany launched its independently developed new lipid-lowering drug Baycol (cerivastatin, trade name: “Baystatin”) into the U.S. market, and because of its excellent lipid-lowering effect, more than 2 million prescriptions were written that year. Just when Bayer was confidently preparing to take on the U.S. pharmaceutical giant, something unexpected happened. In 2001, the U.S. FDA Adverse Drug Reaction Monitoring Center received multiple reports of serious adverse side effects of Baycol from across the U.S. In total, more than 400 cases of rhabdomyolysis were found among patients taking this lipid-lowering drug in the U.S., 31 of whom died. Afterwards, Bayer voluntarily withdrew it from the international market. The rhabdomyolysis incident that shocked the world was not caused by the use of Baycol alone, but by the fact that some doctors in the United States and Europe combined another lipid-lowering drug, gemfibrozil, with Baycol in order to bring down patients’ blood lipids as quickly as possible, thus exacerbating the rhabdomyolysis side effects of the latter. Although the mechanism of action of statins causing hepatic and muscular adverse effects is still not elucidated, numerous analyses have shown that the incidence of adverse effects of these drugs is closely related to their blood levels, and that statins are well tolerated when applied alone, with the frequency of deaths due to rhabdomyolysis being 0.19 per million prescriptions for lovastatin, simvastatin, pravastatin, and atorvastatin, respectively In the United States, a total of 3339 rhabdomyolysis events were reported over a 12-year period, of which approximately 58% were associated with the combination of other drugs. With the accumulation of experience in the clinical use of statins and the development of new drugs, the occurrence of serious complications like rhabdomyolysis is gradually decreasing, but the rationality of long-term, general population use is again being questioned. The 2001 WOSCOPS study found that pravastatin may have a reducing effect on new-onset diabetes, while the 2008 JUPITER study suggested that rasuvastatin had an increased risk of new-onset diabetes. Just what are the risks of statins for new-onset diabetes? How are the risks and benefits of statins evaluated in people with cardiovascular disease risk or existing cardiovascular disease? These questions have become a hot topic of interest in recent years. And among the many meta-analyses, the situation regarding postmenopausal women is still unclear. A study with prospective observational follow-up of a large sample of postmenopausal women ultimately concluded that the application of statins causes a risk of new-onset diabetes in postmenopausal women. Despite the shortcomings, the results of this study, which had a large sample size and was corrected for potential confounding factors, reflect a trend that may lead to a revision of the indications and contraindications for statins. This study also demonstrates that the increased risk of new-onset diabetes caused by statins is a drug-like effect, independent of the potency and type of statin. The finding that women with or without a history of cardiovascular disease were equally likely to develop diabetes with or without statins is indirect evidence that some medications used to treat a history of cardiovascular disease and co-morbid cardiovascular disease conditions may not play a role in the risk of diabetes from statins. A 2009 meta-analysis of six studies of lipid-lowering drugs noted that the risk of diabetes was not statistically different from statin therapy [RR 1.06, CI (0.93-1.25)], but excluding data from the WOSCOPS trial, statins caused a mild and statistically significant increase in the risk of diabetes. a well-known meta-analysis published in 2010 included 13 large clinical trials including 91,140 subjects with a mean follow-up of 4 years. The results showed that the risk of new-onset diabetes was 4.9% and 4.5% in the statin-treated and control groups, respectively, and that statin therapy increased the risk of new-onset diabetes by 9%. The risk of new-onset diabetes was higher with statin therapy in older patients, independent of body mass index and low-density lipoprotein alteration levels. In terms of possible mechanisms for the increased risk of new-onset diabetes with statins, it is possible that statins adversely affect glucose metabolism via glucose transporter protein-4 (GLUT-4); it is also thought that statins antagonize calcium channels, thereby inhibiting insulin secretion. It has also been suggested that the slight increased risk may be due to confounding factors, with statin therapy leading to prolonged survival and thus increased diabetes onset, and patients not receiving statins being more likely to change to a healthy lifestyle after a cardiovascular event, thus reducing the risk of diabetes. The results of the study and the results of the meta-analysis showed that statin therapy was associated with an increased risk of diabetes in patients, with a significant correlation in menopausal women. However, its risk was low both in absolute terms and compared to reduced coronary events. Therefore, in patients with moderate to severe cardiovascular risk or cardiovascular disease, current statin therapy should not be changed! The benefits of statins in terms of improving the prognosis of cardiovascular events need to be further weighed against the risks of increased new-onset diabetes. High-risk groups for cardiovascular disease should be recommended, but low-risk groups or those without strong indications, comorbid metabolic syndrome, or a predisposition to diabetes should be cautious in the use of these drugs.