PPARγ in emphysema: blunts the damage and triggers repair?

Abstract

Cigarette smoke is the most common cause of pulmonary emphysema, which results in an irreversible loss of lung structure and function. Th1 and Th17 immune responses have been implicated in emphysema pathogenesis; however, the drivers of emphysema-associated immune dysfunction are not fully understood. In this issue of the JCI, Shan and colleagues found that peroxisome proliferator-activated receptor γ (PPARγ) is downregulated in APCs isolated from the lungs of emphysematous chronic smokers and mice exposed to cigarette smoke. Furthermore, treatment with a PPARγ agonist prevented emphysema development and appeared to reduce emphysema-associated lung volume expansion in mice exposed to cigarette smoke. Further work will need to be done to evaluate the potential of PPARγ agonists to restore lung capacity in emphysematous patients.

• Authors: Neil J Kelly, Steven D Shapiro
• Journal: The Journal of clinical investigation (J Clin Invest) Vol. 124 Issue 3 Pg. 978-80 (Mar 2014) ISSN: 1558-8238 [Electronic] United States
• PMID: 24569365 (Publication Type: Journal Article, Research Support, N.I.H., Extramural, Comment)

Chemical References

• PPAR gamma
• Thiazolidinediones
• ciglitazone

Topics

• Animals
• Emphysema (drug therapy)
• Humans
• PPAR gamma (metabolism)
• Smoking (adverse effects)
• Thiazolidinediones (pharmacology)