Pathogenesis of chronic obstructive pulmonary disease
Rubin M. Tuder and Irina Petrache
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First published November 1, 2012 - More info
J Clin Invest. 2012;122(11):4300–4300. https://doi.org/10.1172/JCI66725.
Copyright © 2012, The American Society for Clinical Investigation.
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Abstract
The current epidemic of chronic obstructive pulmonary disease (COPD) has produced a worldwide health care burden, approaching that imposed by transmittable infectious diseases. COPD is a multidimensional disease, with varied intermediate and clinical phenotypes. This Review discusses the pathogenesis of COPD, with particular focus on emphysema, based on the concept that pulmonary injury involves stages of initiation (by exposure to cigarette smoke, pollutants, and infectious agents), progression, and consolidation. Tissue damage entails complex interactions among oxidative stress, inflammation, extracellular matrix proteolysis, and apoptotic and autophagic cell death. Lung damage by cigarette smoke ultimately leads to self-propagating processes, resulting in macromolecular and structural alterations — features similar to those seen in aging.
Authors
Rubin M. Tuder, Irina Petrache
Original citation: J. Clin. Invest. 2012;122(8):2749–2755. doi:10.1172/JCI60324.
Citation for this corrigendum: J. Clin. Invest. 2012;122(11):4300. doi:10.1172/JCI66725.
During the preparation of the manuscript, the authors provided an incorrect citation for reference 28. The correct reference is below.
28. Kneidinger N, et al. Activation of the WNT/β-catenin pathway attenuates experimental emphysema. Am J Respir Crit Care Med. 2011;183(6):723–733.
The authors regret the error.
Copyright © 2018 American Society for Clinical Investigation
ISSN: 0021-9738 (print), 1558-8238 (online)