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Matrix degradation in renal disease
Author(s) -
JONES Colin
Publication year - 1996
Publication title -
nephrology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.752
H-Index - 61
eISSN - 1440-1797
pISSN - 1320-5358
DOI - 10.1111/j.1440-1797.1996.tb00061.x
Subject(s) - extracellular matrix , matrix metalloproteinase , fibrosis , medicine , pathogenesis , plasminogen activator inhibitor 1 , kidney , plasmin , glomerulosclerosis , pathology , kidney disease , glomerulonephritis , microbiology and biotechnology , plasminogen activator , endocrinology , biology , biochemistry , enzyme , proteinuria
Summary: The histological appearance of the accumulation of glomerular and tubulointerstitial extracellular matrix (ECM) is a characteristic feature of progressive renal disease. the usual processes behind this finding are a combination of relative loss of parenchymal cells with respect to ECM, increased synthesis of ECM and decreased degradation of ECM. the physiology and pathophysiology of matrix degradation form the basis of tissue remodelling in general and have only been specifically studied in relation to renal disease recently. the two major ECM degrading enzyme systems (the matrix metalloproteinase (MMP), tissue inhibitor of the MMP (TIMP) system and the plasminogen activator/plasmin system) and the interaction between these systems and other non‐specific seem to have an important role in the processes causing matrix accumulation in the ageing kidney, focal sclerosis, diabetes, glomerulonephritis with matrix accumulation and tubulointerstitial disease. A pattern of changes in the expression of components of these enzyme‐inhibitor systems marked by increased TIMP‐1, increased plasminogen activator inhibitor‐1, decreased MMP‐1 and MMP‐3, and increased MMP‐2 and MMP‐9 characterized several models of glomerular and tubulointerstitial fibrosis that are associated, and perhaps caused by, transforming growth factor β. A thorough understanding of the processes controlling matrix degradation may not only be necessary to explain the pathogenesis of matrix accumulation but may also be important in attempting to reverse the processes.