The ''retinoid revolution'' has had considerable impact on research ac
tivity in the field of lung development, Postnatal lungs are very sens
itive to dietary retinol (R) deprivation. The trachea and the bronchop
ulmonary tree in R-deficient animals show a striking change in morphol
ogy. The columnar epithelium undergoes keratinizing metaplasia, which
is reversed when R is supplied. The fetal lung develops postnatally to
become one of the most complex organs, characterized by 40 different
cell types, The fetal lungs can accumulate retinyl esters, Before birt
h an unknown signal causes the lowering of these esters, which may be
the source of retinoic acid (RA). The administration of glucocorticoid
s speeds up this process, which in turn is followed by acceleration of
lung maturation, ending postnatally. It is not clear what role, if an
y, the cellular retinoid binding proteins play in this phenomenon, Fet
al lung branching leading to the development of the alveolar tree is a
ccelerated by RA, and so is the expression of some fetal genes coding
for surfactant proteins and the enzymes that produce their lipid compo
nents, It is not clear whether RA influences the development of pulmon
ary epithelium by interacting directly with the epithelial cells or wh
ether its effects require interaction with other cells like mesenchyma
l cells, Nuclear RA receptors are intimately involved in lung developm
ent, Despite the wealth of evidence on the effect of retinoids on lung
development, the application of vitamin A to clinical work has been L
imited to prematurely delivered infants who have immature lungs. Here
attempts are made, by improving their R status, to aid in the developm
ent and healing of lungs injured by oxygen therapy.