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© 2005 The American Thoracic Society
Peroxisome Proliferator-activated Receptor-
as a Regulator of Lung Inflammation and Repair
Division of Pulmonary and Critical Care Medicine, Department of Internal Medicine, University of Michigan Medical Center, Ann Arbor, Michigan
Correspondence and requests for reprints should be addressed to Theodore J. Standiford, M.D., 6301 MSRB III, 1150 West Medical Center Drive, Ann Arbor, MI 48109. E-mail: tstandif{at}umich.edu
ABSTRACT
Peroxisome proliferator-activated receptors (PPARs) are members of the nuclear hormone receptor superfamily that regulate the expression of genes involved in a variety of biological processes, including lipid metabolism and insulin sensitivity. Members of the PPAR family—in particular, PPAR-
—have more recently been shown to broadly regulate inflammatory and reparative responses. PPAR- is expressed in both alveolar macrophages and neutrophils, and the ligand-dependent activation of this receptor results in suppression of leukocyte effector responses, including cytokine production, the elaboration of reactive oxygen and nitrogen species, and migratory responses. In addition to antiinflammatory effects, PPAR- regulates diverse processes in lung stromal/parenchymal cells, including cell growth, differentiation, and apoptosis. Studies examining in vivo effects of PPAR- have produced complex and at times conflicting results. However, evidence to date generally suggests that PPAR- functions to dampen inflammation and injury in various animal models of acute lung injury. PPAR- may also play an important role in other inflammatory/immune lung diseases, including ischemia-reperfusion injury, allergic airway inflammation, and cancer. The role of PPAR- in human lung diseases, including acute lung injury, requires further study.
Key Words: transcriptional factors • ARDS • gene regulation
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