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Cigarette Smoke Triggers Code Red

p21^{CIP1/WAF1/SDI1} Switches on Danger Responses in the Lung

¹ Department of Medicine, Division of Pulmonary Sciences and Critical Care Medicine, Program in Translational Lung Research, and ² Department of Pathology, University of Colorado Denver, School of Medicine, Denver, Colorado

Correspondence and requests for reprints should be addressed to Rubin M. Tuder, M.D., Division of Pulmonary Sciences and Critical Care Medicine, Department of Medicine, University of Colorado Denver, School of Medicine, 4200 East 9th Avenue, Campus Box C272, Denver, CO 80262. E-mail: Rubin.Tuder{at}UCHSC.EDU

The article by Yao and coworkers in this issue (Am. J. Respir. Cell Mol. Biol. 2008;39:7–18) reveals that the cyclin-dependent kinase inhibitor p21CIP1/WAF1/SDI1 (designated hereafter as p21), which has been linked to cell cycle growth arrest due to stress or danger cell responses, may modulate alveolar inflammation and alveolar destruction, and thus enlightens our present understanding of how the lung senses injury due to cigarette smoke and integrates these responses with those that activate inflammatory pathways potentially harmful to the lung (1). Furthermore, the interplay of p21 and cellular processes involving cell senescence and the imbalance of cell proliferation/apoptosis may provide us with a more logical explanation of how p21, acting as a sensor of cellular stress, might have such potent and wide roles in lung responses triggered by cigarette smoke. Molecular switches, ontologically designed for the protection of the host, are now hijacked by injurious stresses (such as cigarette smoke), leading to organ damage.

Related articles in AJRCMB:

Disruption of p21 Attenuates Lung Inflammation Induced by Cigarette Smoke, LPS, and fMLP in Mice

Hongwei Yao, Se-Ran Yang, Indika Edirisinghe, Saravanan Rajendrasozhan, Samuel Caito, David Adenuga, Michael A. O'Reilly, and Irfan Rahman
AJRCMB 2008 39: 7-18. [Abstract] [Full Text]