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Physiological Reviews, Vol. 81, No. 3, July 2001, pp. 999-1030
Copyright ©2001 by the American Physiological Society
Center for Cardiovascular Research, University of Rochester, Rochester, New York
Berk, Bradford C.
Vascular Smooth Muscle Growth: Autocrine Growth
Mechanisms. Physiol. Rev. 81: 999-1030, 2001.
Vascular smooth muscle cells (VSMC) exhibit several growth
responses to agonists that regulate their function including
proliferation (hyperplasia with an increase in cell number),
hypertrophy (an increase in cell size without change in DNA content),
endoreduplication (an increase in DNA content and usually size), and
apoptosis. Both autocrine growth mechanisms (in which the individual
cell synthesizes and/or secretes a substance that stimulates that same cell type to undergo a growth response) and paracrine growth mechanisms (in which the individual cells responding to the growth factor synthesize and/or secrete a substance that stimulates neighboring cells
of another cell type) are important in VSMC growth. In this review I
discuss the autocrine and paracrine growth factors important for VSMC
growth in culture and in vessels. Four mechanisms by which individual
agonists signal are described: direct effects of agonists on their
receptors, transactivation of tyrosine kinase-coupled receptors,
generation of reactive oxygen species, and induction/secretion of other
growth and survival factors. Additional growth effects mediated by
changes in cell matrix are discussed. The temporal and spatial
coordination of these events are shown to modulate the environment in
which other growth factors initiate cell cycle events. Finally, the
heterogeneous nature of VSMC developmental origin provides another
level of complexity in VSMC growth mechanisms.
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