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Eicosanoid Lipid Mediators in Fibrotic Lung Diseases*: Ready for Prime Time?

Steven K. Huang, MD; Marc Peters-Golden, MD
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*From the Division of Pulmonary and Critical Care Medicine, University of Michigan Medical School, Ann Arbor, MI.

Correspondence to: Marc Peters-Golden, MD, Division of Pulmonary and Critical Care Medicine, 1150 W Medical Center Dr, 6301 MSRB III, Ann Arbor, MI 48109; e-mail: petersm@umich.edu



Chest. 2008;133(6):1442-1450. doi:10.1378/chest.08-0306
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Recognition of a pivotal role for eicosanoids in both normal and pathologic fibroproliferation is long overdue. These lipid mediators have the ability to regulate all cell types and nearly all pathways relevant to fibrotic lung disorders. Abnormal fibroproliferation is characterized by an excess of profibrotic leukotrienes and a deficiency of antifibrotic prostaglandins. The relevance of an eicosanoid imbalance is pertinent to diseases involving the parenchymal, airway, and vascular compartments of the lung, and is supported by studies conducted both in humans and animal models. Given the lack of effective alternatives, and the existing and emerging options for therapeutic targeting of eicosanoids, such treatments are ready for prime time.

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