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Am J Respir Crit Care Med. 2018 Sep 13. doi: 10.1164/rccm.201806-1166PP. [Epub ahead of print]

Why an Aging Smoker Lung Develops IPF and Not COPD?

Author information

1
Instituto Nacional de Enfermedades Respiratorias, Mexico DF, Mexico ; mselmanl@yahoo.com.mx.
2
Cornell Medical College, New York, New York, United States.
3
Universidad Nacional Autónoma de México, Facultad de Ciencias, México DF, Mexico.

Abstract

Idiopathic pulmonary fibrosis (IPF) and chronic obstructive pulmonary disease (COPD) are generally progressive and irreversible chronic-degenerative disorders. COPD is associated with chronic inflammation, and changes in both the alveolar and airway compartments, resulting in small airways disease and emphysema. IPF is driven by an abnormal activation of the alveolar lung epithelium resulting in progressive scarring of the lung parenchyma. Both diseases are heterogeneous with several clinical phenotypes, and usually occur in aged individuals, mostly smokers. Although drastically different but similarly devastating, COPD and IPF share a number of accelerating lung aging processes, smoking injury and even some convergent molecular pathways. A key question remains why an older smoking individual develops IPF instead of COPD? Moreover, why do some individuals develop both diseases? Here we examine the common and divergent pathogenic mechanisms, highlighting the distinct relevant self-determining molecular mechanisms that made the pathological pathways and outcome radically different.

KEYWORDS:

IPF. COPD, genetic architecture, developmental pathways

PMID:
30211626
DOI:
10.1164/rccm.201806-1166PP

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