**7. Conclusion**

Reduction of LDL-C, the main target of hypolipidemic therapy, has been proved effective reducing morbidity and mortality associated to CVD. However, a high proportion of patients receiving statins, the most lipid-lowering family of drugs used, do not reach optimal LDL-C levels. In addition, even in those patients reaching the optimal LDL-C levels following statin treatment, a residual risk remains, probably due to the presence of other risk factors, including the presence of atherogic dyslipidemia (described by the presence of high triglycerides, low HDL-C levels, and the presence of small dense LDL particles), glucose metabolism alterations and additional non-lipid-related risk factors. Several studies have confirmed that PPARβ/δ plays an important role in the regulation of lipoprotein metabolism, leading to reductions in the levels of plasma triglycerides and LDL-C and increases in HDL-C in different animal models. Taken together, these effects attained following PPARβ/δ activation on lipoprotein metabolism are so promising that this nuclear receptor has been considered a therapeutic target to prevent and treat dyslipidemia. However, as with any drug designed for human therapy, a great deal of research will be needed on the efficacy and safety of PPARβ/δ activators before they reach clinical use.
