Περίληψη:
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.
Συγγραφείς:
Li, XP
Shu, RJ
Filippatos, G
Uhal, BD
