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Editorial |

Alveolar Type 2 Cell Transplantation in IPF: Recreating the Silver Lining

Namrata B. Patel, MD; Jason D. Christie, MD, FCCP
Author and Funding Information

FINANCIAL/NONFINANCIAL DISCLOSURES: The authors have reported to CHEST the following: N. B. T. has served as a consultant for InterMune. J. D. C. has received institutional funding from BristolMyersSquibb for an epidemiological study of pulmonary fibrosis.

Pulmonary, Critical Care, and Allergy Division, Perelman School of Medicine at the University of Pennsylvania, Philadelphia, PA

CORRESPONDENCE TO: Namrata Patel, MD, Pulmonary, Critical Care, and Allergy Division, Perelman School of Medicine at the University of Pennsylvania, 831 Gates Bldg, 3400 Spruce St, Philadelphia PA, 19104


Copyright 2016, American College of Chest Physicians. All Rights Reserved.


Chest. 2016;150(3):481-482. doi:10.1016/j.chest.2016.05.036
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Extract

After decades of failed therapies, mechanistic insights have led to the development of therapies successful in curtailing, but not abrogating, the fibrosis that results in the devastating clinical course of patients with idiopathic pulmonary fibrosis (IPF). Alveolar epithelium undergoing injury from various agents such as inhalation exposures, gastroesophageal reflux, DNA viruses, and mechanisms of oxidative stress can stimulate stress response pathways, mediator release, and apoptosis. This abnormally activated epithelium is thought to promote fibroblast recruitment and activation, which leads to matrix deposition and fibroblast persistence. It follows that there is a growing interest in creating cell-based therapies to help restore a normal wound-healing response.

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