Peroxisome proliferator–activated receptors (PPAR) are ligand-inducible transcription factors that belong to the nuclear receptor family. They include three major subtypes: PPAR, PPAR/, and PPAR. Initially, PPAR was identified as the molecular target for the hypolipidemic fibrate drugs that induce peroxisome proliferation in rodents, which explains its name. Further studies have demonstrated that PPAR also bind endogenous ligands such as fatty acids and fatty acid derivatives provided by the lipoxygenase and cyclooxygenase pathways, PPAR being a particular target for polyunsaturated fatty acids such as linoleic acid, dodecahexanoic acid, and eicosapentaenoic acid. After activation by their ligands, PPAR form heterodimers with the retinoic receptor RXR and interact with peroxisome proliferator response element present in the promoter of their target genes. By this transcriptional mechanism, PPAR increases the activity of enzymes that are involved in fatty acid-oxidation, lowering triglyceride levels in vivo. Thus, it would not be surprising if PPAR is expressed in tissues involved in fatty acid oxidation, including liver, kidney, heart, skeletal muscle, and brown fat. Within the kidney, PPAR is predominantly present in proximal tubules and medullary thick ascending limbs. 1

Besides its role in the regulation of energy homeostasis, PPAR has a pivotal role in tissue inflammation and repair. PPARis upregulated by anti-inflammatory glucocorticoids, and, in turn, engagement of PPAR exerts anti-inflammatory effects, acting mainly at the level of the vascular wall and the liver. 2, 3 Underlying cellular and molecular mechanisms involve an interference with inflammatory gene transcription through an interaction of PPAR with co-factors, a decrease in levels of transcription factors, an inhibition of nuclear translocation of transcription factors, and a direct interaction