Recent studies using animal models of glomerulonephritis indicate that steady-state levels of mRNAs encoding basement membrane proteins are frequently, but not universally, increased in parallel and that mRNAs encoding interstitial matrix proteins represent a separate set of genes that may also display coordinate regulation. A variety of maneuvers that ameliorate progressive glomerulosclerosis may act, at least in part, by suppressing glomerular cell matrix protein gene expression. The observed coordinate regulation of matrix genes may be a consequence of shared genetic regulatory sequences. Future therapies designed to retard glomerulosclerosis may take advantage of similarities among the extracellular mediators and regulatory sequences that influence matrix gene expression.