PPARα as a therapeutic target in inflammation-associated diseases.

Introduction: The nuclear receptor peroxisome proliferator-activated receptor alpha (PPARα) plays a major regulatory function of genes involved in energy metabolism and is a therapeutic target for dyslipidemia. The last decade provided a constellation of findings demonstrating that PPARα behaves as a modulator of both acute and chronic inflammation. PPARα became a rational potential therapeutic target for the treatment of inflammatory disorders.

Atheroprotective effect of human apolipoprotein A5 in a mouse model of mixed dyslipidemia.

Hypertriglyceridemia is an independent risk factor for coronary artery disease. Because apolipoprotein (Apo)A5 regulates plasma triglyceride levels, we investigated the impact of human (h)ApoA5 on atherogenesis. The influence of hApoA5 transgenic expression was studied in the ApoE2 knock-in mouse model of mixed dyslipidemia.

Systemic and distal repercussions of liver-specific peroxisome proliferator-activated receptor-alpha control of the acute-phase response.

The acute-phase response is characterized by the modulation of liver expression of many proteins involved in a diversity of biological functions. Among them, some are associated with the pathology of atherosclerosis. We previously found that peroxisome proliferator-activated receptor-alpha (PPARalpha) agonists attenuate the IL-6 induction of acute-phase response gene expression in vitro and in vivo.