Medicine. PPARs as therapeutic targets: reverse cardiology?

Science. 2003 Oct 17;302(5644):406-7. doi: 10.1126/science.1091172.

Abstract

Formation of the atherosclerotic lesions that lead to myocardial infarction is determined in part by inflammatory responses such as the production of lipid-laden macrophages. In his Perspective, Plutzky highlights the parts played by PPAR nuclear receptors, especially PPAR-delta (Lee et al.), in the modulation of inflammatory responses and hence atherosclerosis.

Publication types

  • Comment

MeSH terms

  • Animals
  • Arteriosclerosis / drug therapy
  • Arteriosclerosis / etiology*
  • Arteriosclerosis / metabolism
  • Cytokines / genetics
  • DNA-Binding Proteins / metabolism
  • Foam Cells / physiology
  • Gene Expression Regulation
  • Inflammation / etiology*
  • Ligands
  • Lipoprotein Lipase / metabolism
  • Liver X Receptors
  • Macrophages / physiology*
  • Membrane Glycoproteins / metabolism
  • Mice
  • Orphan Nuclear Receptors
  • Proto-Oncogene Proteins / metabolism
  • Proto-Oncogene Proteins c-bcl-6
  • Receptors, Cell Surface / metabolism
  • Receptors, Cytoplasmic and Nuclear / genetics
  • Receptors, Cytoplasmic and Nuclear / metabolism*
  • Toll-Like Receptors
  • Transcription Factors / genetics
  • Transcription Factors / metabolism*
  • Transcription, Genetic

Substances

  • Cytokines
  • DNA-Binding Proteins
  • Ligands
  • Liver X Receptors
  • Membrane Glycoproteins
  • Orphan Nuclear Receptors
  • Proto-Oncogene Proteins
  • Proto-Oncogene Proteins c-bcl-6
  • Receptors, Cell Surface
  • Receptors, Cytoplasmic and Nuclear
  • Toll-Like Receptors
  • Transcription Factors
  • Lipoprotein Lipase