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The Role of PPARγ in Pulmonary Vascular Disease
  1. C. Michael Hart, MD
  1. From the Atlanta Veterans Affairs and Emory University Medical Centers, Atlanta, GA.
  1. Supported by grants from the Veterans Affairs Research Service, the National Institutes of Health, and Takeda Pharmaceuticals.
  2. The proceedings of a symposium presented at the Experimental Biology Meeting in Washington, DC, on Sunday, April 29, 2007.
  3. Reprints: C. Michael Hart, MD, Emory University, Pulmonary Section, Atlanta Veterans Affairs Medical Center, 1670 Clairmont Rd (151-P), Decatur, GA 30033. E-mail: Michael.hart3{at}va.gov.

Abstract

The peroxisome proliferator-activated receptor (PPAR) γ is a member of the nuclear hormone receptor superfamily of ligand-activated transcription factors. Thiazolidinediones, pharmacological ligands for PPARγ, are currently used in the management of type 2 diabetes. Peroxisome proliferator-activated receptor γ is expressed in the lung and pulmonary vasculature, and its expression is reduced in the vascular lesions of patients with pulmonary hypertension. Furthermore, thiazolidinedione PPARγ ligands reduced pulmonary hypertension and vascular remodeling in several experimental models of pulmonary hypertension. This report reviews current evidence that PPARγ may represent a novel therapeutic target in pulmonary hypertension and examines studies that have begun to elucidate mechanisms that underlie these potential therapeutic effects.

Key Words
  • PPARγ
  • pulmonary hypertension
  • nitric oxide
  • NADPH oxidase

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