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J Appl Physiol 97: 1535-1542, 2004; doi:10.1152/japplphysiol.00519.2004
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INVITED REVIEW

HIGHLIGHTED TOPICS
Lung Growth and Repair

Apoptosis in lung injury and remodeling

Xiaopeng Li,1 Ruijie Shu,1 Gerasimos Filippatos,2 and Bruce D. Uhal1

1Department of Physiology, Michigan State University, East Lansing, Michigan 48824; and 2Second Department of Cardiology, University of Athens, University Hospital, GR11562 Athens, Greece

The mode of cell death termed apoptosis, sometimes referred to as programmed cell death, is as critical a determinant of cell population size as is cell proliferation. Although best characterized in cells of the immune system, apoptosis is now known to be a key factor in the maintenance of normal cell turnover within structural cells in the parenchyma of virtually every organ. Recent interest in apoptosis in the lung has sparked a surge of investigations designed to determine the roles of apoptosis in lung development, injury, and remodeling. Of particular recent interest are the roles of apoptosis in disease pathogenesis and resolution, in which the concept of apoptosis as a "programmed" cell death, i.e., genetically determined, is often more accurately viewed as "inappropriate cell suicide" with regard to its extent and/or timing. Data accumulating over the past decade have made clear the complexity of the control of lung cell apoptosis; concepts of the regulation of apoptosis originally determined in classical cell culture models are often, but not always, applicable to structural cells. For this reason, each of the many cell types of the lung must be studied as a potentially new subject with its own idiosyncrasies yet to be discovered. In light of the large volume of literature now available, this article focuses on the roles of apoptosis in three pathophysiological contexts: acute respiratory distress syndrome, chronic obstructive pulmonary disease, and pulmonary fibrosis. Each section presents key data describing the evidence for apoptosis in the lung, its possible relevance to disease pathogenesis, and proposed mechanisms that might suggest potential avenues for therapeutic intervention.

programmed cell death; acute respiratory distress syndrome; chronic obstructive pulmonary disease; pulmonary fibrosis; caspases



Address for reprint requests and other correspondence: B. D. Uhal, Dept. of Physiology, Michigan State University, 3185 Biomedical and Physical Sciences Bldg., East Lansing, MI 48824 (E-mail: uhal{at}msu.edu).




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