The peroxisome proliferator-activated receptor alpha (PPARα) is a ligand-activated transcription factor involved in regulating various biological processes, including inflammation, immunity, nutrient metabolism, and energy homeostasis. It serves as a molecular target for hypolipidemic fibrates, which bind the receptor with high affinity. PPARα is also activated by numerous fatty acids and fatty acid-derived compounds. PPARα regulates biological processes by altering the expression of a large number of target genes. This review provides an overview of the involvement of PPARα in lipid metabolism and other pathways through a detailed analysis of known or putative PPARα target genes. The emphasis is on gene regulation by PPARα in the liver, although many results likely apply to other organs and tissues. PPARα was first discovered in the early 1990s and has been identified as the master regulator of hepatic lipid metabolism. It has been shown to govern glucose metabolism, lipoprotein metabolism, liver inflammation, amino acid metabolism, and hepatocyte proliferation. Synthetic agonists of PPARα lower plasma triglycerides and raise plasma high-density lipoprotein (HDL) levels and are used clinically in the treatment of dyslipidemia. Recent advances in microarray technology have allowed the study of whole genome expression profiles, providing new insights into the role of PPARα in gene expression. This paper aims to provide a detailed and updated overview of PPARα. PPARα is highly expressed in the liver and other tissues with high fatty acid catabolism rates, such as the heart, kidney, intestine, and brown adipose tissue. It is also expressed in immune cells such as T-cells and macrophages. PPARα expression profiles in mice and humans are similar. PPARα has been most extensively studied in the liver, so most information on PPARα target genes relates to hepatic gene regulation. PPARα has a domain structure consisting of an N-terminal activating function-1 (AF-1) domain, a central DNA-binding domain (DBD), and a C-terminal ligand-binding domain (LBD). Human and murine PPARα show 85% nucleotide and 91% amino acid identity. Genetic heterogeneity in the functional coding sequence of human PPARα leads to functional differences in receptor activity. A variant of the human PPARα gene produces a protein with a mutated DNA-binding domain, which exhibits greater ligand-induced activity. PPARα serves as a receptor for a structurally diverse set of compounds, including fibrates, plasticizers, insecticides, and natural ligands such as fatty acids and fatty acid derivatives. PPARα is activated by dietary fatty acids and fatty acids generated via de novo lipogenesis. PPARα plays a crucial role in lipid metabolism, including fatty acid oxidation, ketogenesis, and triglyceride storage and lipolysis. It alsoThe peroxisome proliferator-activated receptor alpha (PPARα) is a ligand-activated transcription factor involved in regulating various biological processes, including inflammation, immunity, nutrient metabolism, and energy homeostasis. It serves as a molecular target for hypolipidemic fibrates, which bind the receptor with high affinity. PPARα is also activated by numerous fatty acids and fatty acid-derived compounds. PPARα regulates biological processes by altering the expression of a large number of target genes. This review provides an overview of the involvement of PPARα in lipid metabolism and other pathways through a detailed analysis of known or putative PPARα target genes. The emphasis is on gene regulation by PPARα in the liver, although many results likely apply to other organs and tissues. PPARα was first discovered in the early 1990s and has been identified as the master regulator of hepatic lipid metabolism. It has been shown to govern glucose metabolism, lipoprotein metabolism, liver inflammation, amino acid metabolism, and hepatocyte proliferation. Synthetic agonists of PPARα lower plasma triglycerides and raise plasma high-density lipoprotein (HDL) levels and are used clinically in the treatment of dyslipidemia. Recent advances in microarray technology have allowed the study of whole genome expression profiles, providing new insights into the role of PPARα in gene expression. This paper aims to provide a detailed and updated overview of PPARα. PPARα is highly expressed in the liver and other tissues with high fatty acid catabolism rates, such as the heart, kidney, intestine, and brown adipose tissue. It is also expressed in immune cells such as T-cells and macrophages. PPARα expression profiles in mice and humans are similar. PPARα has been most extensively studied in the liver, so most information on PPARα target genes relates to hepatic gene regulation. PPARα has a domain structure consisting of an N-terminal activating function-1 (AF-1) domain, a central DNA-binding domain (DBD), and a C-terminal ligand-binding domain (LBD). Human and murine PPARα show 85% nucleotide and 91% amino acid identity. Genetic heterogeneity in the functional coding sequence of human PPARα leads to functional differences in receptor activity. A variant of the human PPARα gene produces a protein with a mutated DNA-binding domain, which exhibits greater ligand-induced activity. PPARα serves as a receptor for a structurally diverse set of compounds, including fibrates, plasticizers, insecticides, and natural ligands such as fatty acids and fatty acid derivatives. PPARα is activated by dietary fatty acids and fatty acids generated via de novo lipogenesis. PPARα plays a crucial role in lipid metabolism, including fatty acid oxidation, ketogenesis, and triglyceride storage and lipolysis. It also