Recent evidence suggests that decreased degradation of the glomerular extracellular matrix may contribute to the matrix accumulation that occurs in the progression of chronic renal disease. The presence of matrix metalloproteinases in cultured glomerular cells and possibly in glomeruli in vivo combined with the ability of these proteinases to degrade extracellular matrix components suggests that these proteinases may play important roles in glomerular extracellular matrix degradation. Decreased activity of these proteinases mediated by upregulation of their inhibitors could theoretically contribute to matrix accumulation. In the limited number of studies that have addressed this issue directly, there is evidence both to support and refute this hypothesis. It is reasonable to suspect, however, that either increased matrix formation, decreased matrix degradation, or both, might contribute to extracellular matrix accumulation in progressive renal disease, depending on the primary etiology.
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