Glomerular mesangial cells play a central role in maintaining structure and
function of the glomerular capillary ultrafiltration apparatus. Under phys
iological and pathological conditions, mesangial cells regulate amount and
composition of the surrounding extracellular matrix. Conversely, components
of the embedding matrix affect the mesangial cell phenotype. These interac
tions are mediated via specific cell surface receptors, the best studied gr
oup of which is the beta(1) integrin family. The beta(1) integrins play a r
ole in mesangial cell adhesion, migration, survival and proliferation. Expr
ession and abundance of integrins in healthy and diseased glomeruli and the
ir functions and mediation of signals are discussed in this review. Other f
actors modulating mesangial cell-matrix interactions, such as antiadhesive
proteins, cytokines, disintegrins and nitric oxide, are also considered. Th
e available evidence from in vitro and in vivo studies indicates that recep
tor-mediated interactions between mesangial cells and the normal or abnorma
l extracellular matrix regulate the mesangial cell phenotype and thus contr
ibute to normal maintenance of the glomerulus and to remodeling and repair
of the glomerular capillary tuft in response to injury.