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Ubiquitination and Proteolysis in Acute Lung InjuryUbiquitination in Acute Lung Injury

István Vadász, MD; Curtis H. Weiss, MD; Jacob I. Sznajder, MD, FCCP
Author and Funding Information

From the Department of Internal Medicine (Dr Vadász), University of Giessen Lung Center, Justus Liebig University, Giessen, Germany; and the Division of Pulmonary and Critical Care Medicine (Drs Weiss and Sznajder), Northwestern University, Feinberg School of Medicine, Chicago, IL.

Correspondence to: István Vadász, MD, Department of Internal Medicine, University of Giessen Lung Center, Justus Liebig University, Klinikstrasse 33, 35392 Giessen, Germany; e-mail: istvan.vadasz@innere.med.uni-giessen.de


Funding/Support: Research in the authors’ laboratories addressing ubiquitination was supported by the Deutsche Forschungsgemeinschaft [Grant DFG/IRTG1062] to Drs Vadász and Sznajder, the University Medical Center Giessen and Marburg [Grant 62589064] to Dr Vadász, and the National Institutes of Health [Grants HL-71643, R37 48129, HL-85534, and HL-T32 76139] to Drs Weiss and Sznajder. Dr Vadász is supported by the Else Kröner Memorial Award, and Dr Weiss is the recipient of Parker B. Francis Fellowship.

Reproduction of this article is prohibited without written permission from the American College of Chest Physicians (http://www.chestpubs.org/site/misc/reprints.xhtml).


© 2012 American College of Chest Physicians


Chest. 2012;141(3):763-771. doi:10.1378/chest.11-1660
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Ubiquitination is a posttranslational modification that regulates a variety of cellular functions depending on timing, subcellular localization, and type of tagging, as well as modulators of ubiquitin binding leading to proteasomal or lysosomal degradation or nonproteolytic modifications. Ubiquitination plays an important role in the pathogenesis of acute lung injury (ALI) and other lung diseases with pathologies secondary to inflammation, mechanical ventilation, and decreased physical mobility. Particularly, ubiquitination has been shown to affect alveolar epithelial barrier function and alveolar edema clearance by targeting the Na,K-ATPase and epithelial Na+ channels upon lung injury. Notably, the proteasomal system also exhibits distinct functions in the extracellular space, which may contribute to the pathogenesis of ALI and other pulmonary diseases. Better understanding of these mechanisms may ultimately lead to novel therapeutic modalities by targeting elements of the ubiquitination pathway.

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