Abstrakt
Blood pressure, low-density lipoprotein cholesterol (LDL-C), and glycemia (for microvascular disease) represent the triumvirate of targets for managing vascular risk in type 2 diabetes [1]. Novel treatments that substantially lower LDL-C levels [2,3], or that improve glucose control [4e6], can provide additional vascular risk reduction.
Despite these advances in best care, however, an unacceptably high residual cardiovascular risk persists. Therefore, therapeutic interventions aimed at additional targets are needed.
A key contender to address the enigma of residual vascular risk is the nuclear receptor peroxisome proliferator-activated receptor alpha (PPARa). PPARa, which is predominantly expressed in metabolically active tissues, pivotally regulates key metabolic and inflammatory pathways [7,8].
Critical to this role is the ability of PPARa to exert either positive or negative control over the expression of genes involved in fatty acid oxidation, lipoprotein metabolism, and inflammation.